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DISEASES   OF   THE    HEART 

AND 

ARTERIAL   SYSTEM 


DESIGNED    TO  BE  A  PRACTICAL  PRESENTATION  OF 

THE  SUBJECT  FOR    THE   USE   OF  STUDENTS 

AND   PRACTITIONERS  OF  MEDICINE 


BY 
ROBERT    H.    BABCOCK,    A.M.,    M.D. 

Former  Professor  of  Clinical  Medicine  and  Diseases  of  the  Chest,  College  of  Physicians  and  Sur- 
geons (Medical  Department  of  the  Illinois  State  University),  Chicago;  Consulting  Physician 
to  Cook  County  Hospital,  Passavant  Hospital,  Mary  Thompson   Hospital,   Hospital 
of   St.  Anthony  de   Padua,  and   of   Marion-Sims  Sanitarium ;    Member   of   the 
Association   of   American   Physicians,  American    Climatological   Associa- 
tion,  American   Medical   Association,  National  Association  for  the 
Study  and  Prevention  of  Tuberculosis;   Corresponding  Mem- 
ber of  Medico-Chirurgical  Society  of  Edinburgh,  etc. 


WITH    THREE    COLOURED    PLATES    AND 
ONE    HUNDRED    AND   THIRTY-NINE    ILLUSTRATIONS 


THIRD   EDITION,    REVISED 


NEW   YORK   AND   LONDON 

D.    APPLETON    AND    COMPANY 

1910 


6// 


Copyright.  1903,  1905,  1909, 
By  D.  APPLETON  AND  COMPANY 


rUINTKO   AT   THK    APIT.KTON    PKKSS, 
NKW    YORK,    U.    K.    A. 


PREFACE   TO   THE   THIRD   EDITION 


The  changes  in  tins  third  edition  are  not  numerons,  but  arc 
such  as  were  needed  to  bring  certain  portions  of  this  work  up  to 
date.  Accordingly,  the  article  upon  Stokes-Adams  disease  has 
been  entirely  rewritten  so  as  to  conform  with  our  recently  acquired 
knowledge  concerning  heart-block  and  its  relation  to  the  Stokes- 
Adams  syndrome.  An  addition  has  been  made  also  to  the  original 
contribution  by  Dr.  Otto  Schmidt  upon  Gaertner's  tonometer  and 
its  use  in  clinical  medicine.  These  additional  pages  will  be  found 
under  the  caption  of  The  SjDhygmomanometer,  since  instruments 
known  by  this  generic  appellation  have  supplanted  the  tonometer 
of  Gaertner  and  the  instrument  of  von  Basch  in  the  United  States. 
Finally,  a  few  foot-notes  and  corrections  have  been  made  which 

it  is  believed  increase  the  value  of  the  text. 

R.  H.  B. 


PEEFACE   TO   THE   SECOND   EDITION 


The  changes  made  in  this  second  edition  while'  not  numerous 
and  not  affecting  the  work  as  a  whole  are  yet  important.  In  the 
main  they  concern  that  form  of  insufficiency  of  the  auriclo-ven- 
tricular  valves  which  depends  not  ujx)n  endocarditis  but  upon 
alterations  of  the  myocardium,  and  in  the  former  edition  was 
regarded  as  always  relative.  In  this  one  the  author  believes  he 
has  given  due  recognition  to  that  variety  of  mitral  and  tricuspid 
incompetence  termed  muscular.  Hence  a  portion  of  Chapter 
XXII  has  been  entirely  rewritten,  while  allusions  to  muscular 
insufficiency  have  been  introduced  here  and  there  in  other  chap- 
ters. The  work  has  been  enhanced  in  value  thereby  and  has 
been  brought  strictly  up  to  date. 

R.  n.  B. 


PREFACE 


In  the  preparation  of  this  work  the  author  has  endeavoured 
to  present  the  subject  in  a  simjDle,  practical  fashion  that  would 
suit  the  needs  of  the  student  and  practitioner  of  medicine.  The- 
ories and  speculations  have  been  omitted  or  given  but  scanty 
consideration,  in  the  belief  that  they  tend  to  confuse  the  student. 
The  anatomy  and  physiology  of  the  circulatory  organs  have  re- 
ceived only  such  notice  as  was  thought  necessary  to  a  better  un- 
derstanding of  the  matter  in  hand,  since  an  extended  consideration 
of  them  was  believed  out  of  place  in  a  work  devoted  to  diseased 
conditions.  Although  aware  that  physical  signs  are  properly  a 
part  of  the  symptomatology  of  disease  and  should  be  considered 
under  that  head,  still  the  author  has  thought  it  best  to  consider 
them  separately,  for  the  sake  of  facilitating  the  knowledge  of  that 
most  difficult  subject,  the  diagnosis  of  cardiac  disease.  Special 
attention  has  been  paid  to  treatment,  and  this  part  of  the  subject 
will, be  found  far  more  detailed  than  is  the  case  in  most  books 
dealing  with  diseases  of  the  heart.  It  was  hoped  that  by  so  doing 
the  work  might  be  given  a  more  practical  value  to  the  general 
practitioner,  although  of  course  the  author  realized  that  he  would 
lay  himself  open  to  adverse  criticism,  and  could  do  but  little  more 
than  lay  down  principles  for  management.  The  j)hraseology  has 
been  kept  simple  and  free  from  needless  technicalities,  while  in 
the  terminology  an  attempt  has  been  made  to  employ  the  terms 
which  are  in  most  familiar  use  among  American  and  English 
physicians.     jSTo  claim  is  laid  to  originality,  as  is  apparent  from 


iv  DISEASES  OF  THE   HEART 

the  numerous  references  to  authors  from  whose  works  valnable 
suggestions  and  information  have  been  derived.  To  all  such 
authors,  grateful  acknowledgment  is  made. 

In  conclusion  the  writer  desires  to  express  particular  thanks 
to  the  following  gentlemen :  l)rs.  O.  L.  Schmidt,  for  the  article  on 
Gaertner's  Tonometer ;  Edward  F.  Wells,  for  that  on  the  Sphyg- 
mograph;  Gustav  Fiitterer,  for  anatomical  specimens  and  jDhoto- 
graphs;  W.  A.  Evans,  for  post-mortem  examinations  and  other 
aid ;  and  Milton  W.  Hall,  for  preparing  the  illustrations.  Finally, 
the  author  wishes  to  publicly  express  his  indebtedness  to  his  wife, 
for  her  encouragement  to  undertake  this  work,  for  her  perusal  of 
his  manuscript,  and  suggestions,  without  which  many  passages 
might  have  been  obscure,  and  for  her  invaluable  aid  in  the  revi- 
sion of  proof. 

ROBEKT    H.    BaBCOCK. 
103  State  Street,  Cuicago,  III. 


CONTENTS 


GENERAL    CONSIDERATIONS    PERTAINING    TO    THE    ANAT- 
OMY, PHYSIOLOGY,  AND  EXAMINATION  OP  THE   HEART 

PAGE 

Introductory 1 

Location  of  the  heart  ............  1 

The  relations  of  the  heart  to  the  anterior  thoracic  wall 2 

Position  of' the  great  vessels  and  valves 3 

Cardiac  percussion        . '  .        .        .        .  5 

Auscultatory  or  stethoscopic  percussion 8 

Palpato7'y  percussion 10 

Auscultation  of  the  heart 12 

Normal  heart-sounds    .         .         . 13 

Meduplieation  of  the  heart-sounds 16 

Reduplication  of  the  first  sound 18 

Gallop  or  canter  rhythm 18 

Murmurs .  21 

Endocardial  murmurs  of  organic  origin 21 

Cardiac  areas 25 

Accidefital  murmurs •         .26 

Musical  murmurs 29 

Accidental  musical  murmurs „         .         .  32 

The  differential  diagnosis  of  accidental  heart  murmur 34 

Exocardial  murmurs .  36 


SECTION   I 

DISEASES  OF   THE   PERICARDIUM 

CHAPTER  I 

ACUTE   PERICARDITIS 

Morbid  anatomy " 37 

Etiology 41 

DRY   PERICARDITIS 

Symptoms ,        c        .        c        .      48 

Course  and  termination       .        ..o        .......      56 

V 


vi  DISEASES  OF   THE   HEART 

PAGE 

Physical  signs.    Inspection ,        c        .  56 

Palpation 57 

Percussion ,        ...  57 

Auscultation 57 

LocatioJi  of  the  jyericnrdial  friction-sound         .        .        ,        .         .        .        .58 

Rlnjthni  of  the  friction-sound      ..........  58 

Intensity  of  the  friction-sound 59 

(Quality  of  the  friction-sound 59 

Effect  of  pressure  on  the  pericardial  uiunuur 59 

Diagnosis 60 

Differential  diagnosis .  60 

Prognosis 61 

PERICARDITIS    WITH    EFFUSION 

Symptoms 65 

Course  and  termination 73 

Physical  signs.     Inspection 74 

Palpation .75 

Percussion .  76 

Atiscultation 79 

Secondary  i)hysical  siyns  referable  to  the  lu)igs 80 

Diagnosis 81 

Differential  diagnosis 82 

Prognosis 84 

Treatment 86 

Treatment  in  the  stage  of  effusion 90 

CHAPTER   II 

CHRONIC    PERICARDITIS 

Morbid  anatomy 100 

Etiology        .    " 103 

Symptoms 104 

Course  and  termination 117 

Physical  signs.    Inspection 118 

Palpation 120 

Percussion 121 

Auscultation 121 

Diagnosis 122 

Prognosis 123 

Treatment 124 

CHAPTER  III 

I.   HYDBOPERICARDIUM 

Morbid  anatomy 127 

Etiology 128 

Symptoms 128 

Physical  signs.     Inspection 128 

Paljjation 128 


Percussion    . 
AtoscuUation 
Diagnosis 
Prognosis 
Treatment    . 


CONTENTS  vii 


120 
129 
129 
129 
130 


II.   H^MOPERICARDIUM 

Morbid  anatomy 130 

Etiology 130 

Symptoms 131 

Physical  signs       . 131 

Diagnosis 131 

Prognosis .  131 

Treatment 131 

III.    PNEUMOPERICARDIUM 

Morbid  anatomy 132 

Etiology 132 

Symptoms 133 

Physical  signs.     Inspection 134 

Percussion 134 

AuscuUcdio?i 134 

Diagnosis 135 

Prognosis 135 

Treatment 135 

IV.    TUBERCULOSIS   OF   THE   PERICARDIUM 

Morbid  anatomy 136 

Etiology 137 

Symptoms 138 

Physical  signs 138 

Diagnosis 138 

Prognosis 138 

Treatment     . 138 

V.    SYPHILIS   OF   THE   PERICARDIUM 

Morbid  anatomy 139 

Etiology 140 

Symptoms 140 

Physical  signs 140 

Diagnosis 141 

Prognosis 141 

Treatment 141 

VI.     CARCINOMA   AND   SARCOMA   OF   THE   PERICARDIUM 

Morbid  anatomy 141 

Etiology 142 

Symptoms 142 

Physical  signs 142 

Diagnosis 142 

Prognosis  and  treatment      .....<,.        o.o        .  142 


Vlll 


DISEASES  OP  THE   HEART 


SECTION  II 

DISEASES  OF  THE  ENDOCARDIUM 

CHAPTER  IV 

ACUTE    ENDOCARDITIS  PAGE 

Morbid  anatomy 144 

Etiology 150 

Simple  endocarditis 152 

Ulcerative  endocarditis 155 

Syni|itoms 157 

Acute  simple  endocarditis 157 

Diagnosis 163 

Course  and  termination 163 

Ulcerative  endocarditis .  163 

Course  and  termination 172 

Physical  signs.    Inspection 176 

Palpation 176 

Percussion 177 

Auscultation 177 

Diagnosis 178 

Diagnosis  ot  ulcerative  endocarditis 179 

Prognosis 183 

Treatment 187 

Treatment  of  acute  ulcerative  endocardilis     .......  191 

CHAPTER  V 


chronic  endocarditis 


Morbid  anatomy 
Etiology 
Symptoms     . 


199 
201 
205 


CHAPTER  VI 


MITRAL    regurgitation 


Morbid  anatomy  . 

Etiology 

Symptouis     . 

Physical  signs.     InsjKction 

I'alpntion 

Percussion    . 

Auscultation 

Diagnosis 

Prognosis 

Mode  and  causes  of  death 


216 
221 
223 
239 
239 
240 
242 
245 
246 
247 


CHAPTER  VII 
mitral  stenosis 


Mf)rbid  anatomy 
Etiology 


249 
252 


CONTENTS  IX 

PACK 

Symptoms 255 

Pliysical  signs.     Inspection 258 

Pidpation 259 

Percussion 260 

Auscultation 261 

Diagnosis 268 

Prognosis 269 

Mode  and  causes  of  death 270 

CHAPTER  VIII 

AORTIC    REGURGITATION 

Morbid  anatomy 278 

Etiology 280 

Symptoms 282 

Physical  signs.     Insjjection 297 

Palpation 298 

Percussion 801 

Diagnosis 305 

Prognosis 306 

Mode  and  causes  of  death 307 

CHAPTER  IX 

AORTIC   STENOSIS 

Morbid  anatomy 319 

Etiology 322 

Symptoms 323 

Physical  signs.     Inspection 335 

Palpation 335 

Percussion 336 

Auscultation 337 

Diagnosis 338 

Prognosis 339 

Mode  and  causes  of  death 340 

CHAPTER  X 

TRICUSPID    REGURGITATION 

Morbid  anatomy 344 

Etiology 345 

Symptoms 347 

Physical  signs.     Inspection 349 

Palpation 350 

Percussion 351 

Diagnosis 353 

Prognosis 354 

Mode  and  causes  of  death 354 

CHAPTER  XI 

TRICUSPID   STENOSIS 

Morbid  anatomy 355 

Etiology 356 


X  DISEASES  OF   THE   HEART 

PAGE 

Symptoms ^">7 

Physical  signs.     Inspection 361 

Percussion 362 

AuscitUation 362 

Diagnosis 363 

Prognosis 364 

Mode  and  causes  of  death 364 

CHAPTER  XII 

PULMONARY    REGURGITATION 

Morbid  anatomy 365 

Etiology 366 

Symptoms 367 

Physical  signs 370 

Inspection 371 

Palpation 371 

Percussion 371 

Auscultation 372 

Diagnosis 373 

Pi'ognosis .  374 

Mode  and  causes  of  death 374 


CHAPTER  XIII 

PULMONARY   STENOSIS 

Morbid  anatomy 376 

Etiology 380 

Symptoms 380 

Physical  signs.     Inspection 385 

Palpation 386 

Percussion 386 

Auscultation 386 

Diagnosis 387 

Prognosis 387 

Mode  and  causes  of  death 388 

Summary  of  physical  signs  of  valve  lesions  of  the  right  heart ....  389 

CHAPTER   XIV 


COMBINED    VALVULAR   LESIONS 


Combined  mitral  stenosis  and  regurgitation 

Symptoms. 

Diagnosis  . 


Prognosis  . 
Mitral  stenosis  anij 
Symptoms. 
Diagnosis  . 
Prognosis  . 


AORTIC    STENOSIS 


390 
391 
391 
392 
392 
392 
392 
393 


CONTENTS 


XI 


PAGE 

Mitral  stenosis  and  aoiitic  regurgitation    <,..,„,.  393 

Symploins 393 

Diagnosis 394 

Inspection .        .        .         .  395 

Palpation , 395 

Percussion 395 

Auscultation 395 

Prognosis 396 

Mitral  regurgitation  and  aortic  stenosis   .......  396 

Symptoms 396 

Diagnosis ,        .        .  396 

Prognosis 396 

Aortic  regurgitation  and  mitral  regurgitation         .        .        ...        .  397 

Symptoms 397 

Diagnosis 397 

Prognosis 398 

Aortic  stenosis  and  aortic  regurgitation    .        .        ,        .        .        .        .  398 

Symptoms 398 

Physical  signs .        .        .        ...  399 

Diagnosis 399 

Prognosis 400 


CHAPTER  XV 
the  prognosis  of  valvular  heart-disease  in  general 

Complications 405 

Rheumatic  diathesis 406 

Digestive  and  bronchial  disorders 407 

Age 407 

Temperament 408 

Sex 409 

Occupation 409 

Habits .   ' 410 

Home  surroundings 410 

The  probable  effect  on  the  patient  of  the  knowledge  of  his  lesion     .        .        .  411 

The  effect  of  digitalis  on  the  patient 411 

The  relation  of  prognosis  to  life  insurance 412 

CHAPTER  XVI 


the  treatment  op  valvular  heart-disease 
Compensation  being  still  perfect 
Exercise    . 
Occupation 
Habits 
Marriage 
Clothing 
Baths 
Food, 
ninesses 
Use  of  drugs 
Change  of  climate,  with. special  reference  to  high  altitude 


414 
414 
419 
430 
422 
425 
427 
428 
429 
430 
433 


xii  DISEASES   OF   THE    HEART 

CHAPTER  XVII 

THE   TREATMENT   OF    VALVULAR    HEART-DISEASE   {continued)  ^^^^ 

II.  Compensation  being  imperfect 435 

Medicinal  agents 444 

Rest ...,.,  448 

Exercise 454 

Resistance  exercise 455 

Naiiiieim  baths 464 

Diet 470 

Clothing,  habits,  occupation 476 

CHAPTER  XVIII 

THE   TREATMENT    OE    VALVULAR    HEART  DISEASE    {conclilded) 

III.  Compensation  lost 478 

The  treatment  of  dropsy 489 

Cathartics 492 

The  use  of  digitalis 494 

Accessory  heart  tonics 499 

Hypnotics 500 

Rest 503 

Exercise 502 

Baths 503 

Receiving  visitors 503 

Diet 503 


SECTION    III 

DISEASES  OP   THE   MYOCARDIUM 

CHAPTER  XIX 

ACUTE    MYOCARUITIS 

Morbid  anatomy 506 

Etiology ,         ...  508 

Symptoms 510 

Physical  signs.     Inspection .        .014 

Pdlpation 514 

Percussion 514 

Auscultation 514 

Diagnosis 514 

Prognosis 515 

Treatment 515 

CHAPTER  XX 

CHRONIC    MYOCARDITIS 

Morbid  anatomy 519 

Etiology 522 


'  CONTENTS 


Xlll 


PAGE 

Symptoms '     .        „        .        .        .        ,  520 

Physical  signs.     Inspection 543 

Palpation 543 

Percussion 544 

A^iscultation 545 

Diagnosis _      ,         .  547 

Prognosis 540 

Treatment 551 

Commencing  loss  of  heart-potver 553 

Cardiac  incompetency  pronounced 555 

CHAPTER  XXI 

HYPERTROPHY    OF    TEE    HEART 

Morbid  anatomy 565 

Etiology ■ 568 

Symptoms 570 

Physical  signs.    Inspection 571 

Palpation 571 

Percussion 571 

Auscxdtation 572 

Diagnosis 572 

Prognosis 574 

Treatment 575 

CHAPTER  XXII 

DILATATION   OF   THE   HEART — RELATIVE   AND   MUSCULAR   MITRAL  INSUFFICIENCY 


I.   DILATATION  OF   THE   HEART 


Morbid  anatomy 

Etiology 

Symptoms    . 

Physical  signs.    Inspection 

Palpation 

Percussion   . 

Auscultation 

Diagnosis 

Prognosis 

Treatment    . 

(1)  Bloodlettitig 

(2)  Naulieim  baths 

(3)  Resistance  exercises 


II.    RELATIVE   AND 


Pathology     . 
Etiology 
Symptoms    . 
Physical  signs 
Diagnosis 
Prognosis    . . 
Treatment    . 


MUSCULAR  MITRAL   INSUFFICIENCY 


576 

577 
580 
585 
585 
585 
586 
586 
587 
590 
591 
592 
592 

595 
596 
597 
597 
597 
598 
598 


xiv  DISEASES  OF   THE   HEART 


CHAPTER  XXIII 

FATTY    UliART — CARDIAC    INADEQUACY    OF    TUE    CORPULENT  p^^.^. 

Morbid  anatomy  .        .  599 

Pathology 599 

Etiology 600 

Symptoms 602 

Physical  signs.    Inspection 604 

Palpation 604 

Percussion 604 

Auscultation 605 

Diagnosis 605 

Prognosis 606 

Treatment 606 

CHAPTER  XXIV 

CARDIAC    ASTHMA — CUEYNE-STOKES    RESPIRATION — BRADYCARDIA — STOKES-ADAMS 

SYNDROME 

I.  Cardiac  asthma 613 

II.  Cheyne-Stokes  respiration 615 

Diseases  in  which  Cheyjie-Stokes  breathing  is  observed         ....  617 

Theories  to  explain  Cheyne-Stokes  respiration 617 

Prognosis 622 

Treatment 623 

III.  Bradycardia 624 

IV.  Stokes- Adams  syndrome 627 

Etiology  and  pathology 027 

Symptoms 629 

Prognosis •        .        .        .        .  635 

Treatment 635 

CHAPTER  XXV 

ANGINA    PECTORIS 

Definition 637 

History 637 

Pathology  and  etiology 640 

Clinical  history  and  features  of  an  attack 649 

Diagnosis 654 

Prognosis 657 

Treatment 658 

CHAPTER  XXVI 

SYPHILIS   OF   THE   MYOCARDIUM — NEW    GROWTHS    IN    THE   MYOCARDIUM — ATROPHY 
OF    THE    HEART — SEGMENTATION    AND    FRAGMENTATION    OF    THE    MYOCARDIUM 


I.  Syphilis  of  the  myocardium 
M(M-ljid  anatomy 
Etiology     .... 
Syin|)ti)ms  .         .         . 

Diagnosis  .... 


663 
663 
663 
664 
664 


CONTENTS  XV 

PAGE 

Prognosis  .        .        .        ,        = 665 

Treatment '....,  665 

II.  New  growths  in  the  myocardium 666 

III.  Atrophy  of  the  heart 667 

Morbid  anatomy .        .        .  667 

Etiology 667 

Symptoms 668 

Diagnosis 668 

Prognosis 668 

Treatment 668 

IV.  Segmentation  and  fragmentation  of  the  myocardium         ....  668 

CHAPTER   XXVII 

PEDUNCULATED  AND  BALL  THROMBI  OF  THE  HEART 

Pathogenesis  and  etiology 674 

Symptoms 675 

Diagnosis ,  677 

Prognosis 678 

Treatment 678 

Bibliography  of  cases  of  ball  thrombi         ........  680 

CHAPTER  XXVIII 

DEXTROCARDIA 

Congenital  dextrocardia       . 681 

Symptoms. 681 

Diagnosis  .....' 682 

Acquired  dextrocardia         .        .        .        .        , 682 

Morbid  anatomy 682 

Etiology .683 

Symptoms 684 

Diagnosis .^ 684 

Inspection  and  2Ml2}ation 684 

Percussion 684 

Auscultation 684 

Prognosis 685 

Treatment 685 

CHAPTER  XXIX 

CONGENITAL   DISEASES   OF   THE   HEART 

Morbid  anatomy  .        .        .        .        .        . 686 

Etiology 689 

Symptoms 690 

Physical  signs.     Insjjection 695 

Palpation 696 

Perctission 697 

Diagnosis 701 

Prognosis 701 

Treatment 702 

2 


xvi  DISEASES  OF  THE   HEART 


SECTION  IV 

CARDIAC  NEUROSES 

Syn.  :  Functional  Disorders  of  the  Heart 

CHAPTER  XXX 

PALPITATION,   TACHYCARDIA,   CARDIAC   PAIN,   PSEUDO-ANGINA   PECTORIS 

PAGE 

Pathology '^'03 

Symptoms • 'J'04 

Palpitation '^04 

Tachycardia 715 

Cardiac  pain '  •        •         •  718 

Pseudo-angina  pectoris 719 

Etiology 722 

Diagnosis 724 

Prognosis 726 

Treatment 727 

Treatment  of  the  attack 727 

Palpitation 727 

The  attack  of  pain 728 

CHAPTER  XXXI 

ESSENTIAL   PAROXYSMAL   TACHYCARDIA 

Pathology 731 

Etiology 732 

Features  of  the  paroxysm 732 

Diagnosis 734 

Prognosis 735 

Treatment 735 


SECTION   V 
DISEASES  OF  THE  ARTERIAL  SYSTEM 

CHAPTER  XXXII 

Arteriosclerosis 738 

Morbid  anatomy 739 

Etiology 741 

Symptoms 745 

Physical  signs 750 

Diagnosis 751 

Prognosis 754 

Treatment 754 


CONTENTS  xvii 


CHAPTER  XXXIII 

ACUTE  AORTITIS  —  ACUTE  ARTERITIS  —  SYPHILITIC  ARTERITIS  —  ENDARTERITIS 
OBLITERANS — PERIARTERITIS  NODOSA — STENOSIS  OF  THE  AORTA  AND  PULMONARY 
ARTERY — CONGENITAL   SMALLNESS   OF   THE   ARTERIES 

I.     ACUTE    AORTITIS  p^^^. 

Morbid  anatomy 759 

Etiology 760 

Symptoms 760 

Physical  signs 761 

Inspection 761 

Palpation 761 

Percussion .' 761 

Auscultation 762 

Diagnosis 763 

Prognosis 762 

Treatment 762 


II.    ACUTE   ARTERITIS 

Morbid  anatomy 762 

Symptoms 763 

Physical  signs.    Inspection — Palpation 763 

Diagnosis 763 

Prognosis , 763 

Treatment 764 

III.     SYPHILITIC   ARTERITIS 

Morbid  anatomy 764 

Etiology 765 

Symptoms 765 

Diagnosis 766 

Prognosis 766 

Treatment     .        .        ,        .        .        ,      ' 766 

IV.     ENDARTERITIS    OBLITERANS 

Morbid  anatomy 766 

Etiology 767 

Symptoms 767 

Diagnosis '    .        . 768 

Prognosis  and  treatment 769 

V.     PERIARTERITIS    NODOSA 

Syn.  :  Congenital  Aneurysm 

Morbid  anatomy 769 

Etiology 769 

Symptoms 769 

Diagnosis 770 

Prognosis  and  treatment 770 


xviii  DISEASES   OF  THE   HEART 

VI,    STENOSIS   OF   THE   AORTA   AND    PULMONARY   ARTERY  ^^^^ 

Stenosis  of  the  aorta,  congenital  and  acquired 770 

Symptoms 771 

Diagnosis '''71 

Prognosis  and  treatment 772 

Stenosis  of  the  pulmonary  artery 772 

Symptoms 772 

Diagnosis 772 

Prognosis  and  treatment 773 

VII.    CONGENITAL   SMALLNESS   OF   THE   ARTERIES 

Symptoms 773 

Diagnosis '74 

Prognosis  and  treatment ■  .        .        .  774 

CHAPTER  XXXIV 

ANEURYSM  OF  THE  THORACIC  AORTA 

Morbid  anatomy 775 

Etiology        . 777 

Symptoms 781 

Pain 782 

Dyspnoea 783 

Cough 784 

Expectoration 784 

Physical  signs.     Inspection 800 

Palpation 801 

Percussion °02 

Auscultation 8Q2 

Diagnosis 804 

Prognosis 808 

Modes  and  causes  of  death 808 

Treatment 809 

APPENDIX 

Mechanical  devices  as  aids  to  determining  cardiac  disease    .        .        .  815 

The  X-ray 815 

The  sphygmograph 818 

Gaertner's  tonometer .        .        .        .        •  8-o 

The  sphygmomanometer ""^^ 


LIST   OF  PLATES  AND   ILLUSTRATIONS 


PLATE 

I.     Anatomical  relations  of  thoracic  and  abdominal  viscera .        .        .        . 
II.     Aortic  regurgitation  with  calcified  vegetation  that  swung  in  blood  cur- 
rent, causing  atheroma  of  endocardium  and  of  intima  of  aorta    . 
III.     Exterior  of  heart  of  Fig.  42,  showing  hypertrophy  and  dilatation  of 
both  ventricles         ......... 


FACINO 
PAGE 


576 


unds  are  most  distinctly  Jieard 


cusps  and 


Cardiac  valve  areas,  showing  ivTiere  so 

Normal  deep-seated  cardiac  dulness 

Auscultatory  percussion 

Hein's  palpatory  percussion 

Ebstein's  palpatory  percussion     . 

Maguire's  palpatory  percussion   . 

Normal  cardiac  cycle    . 

Cardiac  valve  areas,  indicating  sounds  produced  at  various  valves 

Interior  of  left  ventricle,  shoiving  fihrous  land  connecting  aortic 

responsible  for  musical  murmur 

Heart  of  a  buffalo  calf,  shoiving  aberrant  chordce  tendince  in  left  ventricle 

Cor  villosum  of  acute  plastic  pericarditis   .... 

Usual  location  of  pericardial  friction  sound  and  fremitus 

Absolute  dulness  in  ease  of  acute  pericarditis    . 

Case  of  pericarditis  in  which  the  sac  contained  3^  pounds  of  fluid  (Bramwell) 

Absolute  dulness  in  ease  of  pericarditis  with  effusion 

Roteh's  sign  of  beginning  effusion      .... 

Pins  and  Ewart's  signs  of  pericardial  effusion    . 

Apex-beat  and  area  of  cardiac  dulness  in  case  of  pericarditis  with  effusion 

The  various  sites  for  puncture  in  paracentesis  pericardii  . 

Cardiac  dulness  and  location  of  border  of  liver  in  special  cases 

Verrucose  endocarditis  of  aortic  and  mitral  valves    . 

Verrucose  endocarditis 

Malignant  verrucose  endocarditis  of  mitral  valve 

Malignant  verrucose  endocarditis  of  aortic  valve,  with  perforation  of  a  cusp 

Apex-beat  and  relative  dulness  in  case  of  acute  endocarditis 

Apex-beat  and  absolute  dulness  later  in  same  case    . 

Apex-beat  and  relative  cardiac  dulness ;  special  case 

Area  of  maximum  audibility  and  transmission  of  murmur ;  special 

Chart   T.     Temperature  in  case  of  acute  endocarditis 

Chart  II.     Temperature  in  case  of  acute  endocarditis 

Diminution  of  relative  cardiac  dulness  in  one  week  under  treatment 

Relative  dulness  in  case  of  chronic  endocarditis 

Condition  of  mitral  valve  causing  regurgitation  and  obstruction 


108 


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14 

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31 

38 

39 

58 

63 

65 

71 

78 

80 

93 

94 

115 

145 

146 

147 

149 

159 

161 

165 

165 

167 

173 

186 

203 

217 


XX  DISEASES   OP  THE   HEART 

PAQE 

Diagram  showing  effects  of  a  mitral  leak  on  the  circulation     ....  2/JO 

Relative  dulness  in  case  of  mitral  insufficiency 237 

Apex-beat  and  relative  dulness  in  mitral  regurgitation 230 

Sphygmogram,  showing  irregular  pulse  in  case  of  mitral  regurgitation   .        .  240 

Relative  dulness  in  a  typical  case  of  mitral  regurgitation         ....  241 
Point  of  maximum  audibility  and  area  of  transmission  of  mitral  regurgitant 

mui'mur 242 

Time  of  mitral  regurgitant  murmur 243 

Interior  of  left  ventricle,  showing  buttonhole  slit 250 

Case  of  mitral  stenosis,  showing  ascites  and  clubbing  of  finger-tips          ,         .  258 

Sphygmogram,  from  case  of  mitral  stenosis 260 

Location  of  apex-beat  and  area  of  deep-seated  dulness  in  mitral  stenosis         .  260 
Rhythm  of  characteristic  murmur  of  mitral  stenosis,  "  auricular  systolic  "      .  261 
Area  of  audibility  of  the  presystolic  murmur  of  mitral  stenosis        .        .         .  262 
Rhythm  of  occasional  variety  of  mitral  stenotic  murmur  through  entire  ven- 
tricular diastole 264 

"  Interrupted  modified  presystolic  "  murmur  of  mitral  stenosis         .        .        .  265 
Location  of  apex  and  relative  dulness  in  case  of  mitral  stenosis       .        .        .  271 
Location  of  apex  and  relative  dulness  in  case  of  mitral  stenosis  and  regurgi- 
tation       273 

Location  of  apex  and  relative  dulness  in  case  of  mitral  stenosis       .        .        .  276 

Location  of  apex  and  relative  dulness  in  case  of  aortic  regurgitation      .        .  285 

Sphygmogram  of  aortic  regurgitation 299 

Sphygmogram  of  pulsus  bisferiens 300 

Type  of  relative  dulness  in  well-compensated  aortic  regurgitation   .        .        .  302 

Type  of  relative  dulness  in  poorly  compensated  aortic  regurgitation       .        .  302 
Spot  of  maximum   intensity   and  area   of    transmission   of   typical  aortic 

regurgitant  murmur 303 

Rhythm  of  aortic  regurgitant  murmur 303 

Relative  dulness  in  case  of  aortic  regurgitation oil 

Skiagram  of  chest  in  case  of  aortic  regurgitation 312 

Relative  dulness  and  lower  border  of  liver  shortly  before  death        .        .        .  316 

Heart  of  aortic  stenosis  with  adherent  cusps  and  also  acute  endocarditis         .  320 

Heart  of  aortic  stenosis  showing  calcified  vegetations  in  sinuses  of  Valsalva  .  321 

Sphygmogram  from  case  of  aortic  stenosis 329 

Sphygmogram  of  uncomplicated  aortic  stenosis 336 

Typical  relative  dulness  in  case  of  well-compensated  aortic  stenosis         .        .  336 

Rhythm  of  aortic  obstructive  murmur 337 

Place  of  maximum  intensity  and  propagation  of  aortic  stenotic  murmur         .  337 

Relative  dulness  in  case  of  primary  tricuspid  regurgitation      ....  351 
Relative  dulness  in  ease  of  tricuspid  regurgitation  secondary  to  dilatation  of 

right  ventricle 3.52 

Place  of  maximum  audibility  and  area  of  propagation  of  tricuspid  regurgi- 
tant murmur 352 

Location  of  thrill  and  murmur  in  a  typical  case  of  tricuspid  stenosis      .         .  361 
Relative  cardiac  dulness  in  typical  case  of  tricuspid  stenosis    ....  362 
Area  of  deep-seated  cardiac  dulness  in  case  of  pulmonary  regurgitation  .        .  368 
Area  of  maximum  intensity  and  of  propagation  of  murmur  in  case  of  pul- 
monary regurgitation 360 

The  rhythm  of  murmur  in  typical  case  of  puhnonary  regurgitation          .        .  :'.73 

Heart  of  a  boy,  showing  congenital  stenosis  of  the  pulmonary  orifice       .        .  379 


INTRODUCTORY  3 

ity  of  this  triangular  area  is  filled  by  the  pulmonary  artery  and 
the  tip  of  the  left  auricular  appendix  as  it  curves  around  the  outer 
border  of  the  left  ventricle  to  appear  in  front  to  and  terminate 
near  the  trunk  of  the  great  artery.  It  is  obvious,  therefore,  that 
only  the  upper  third  of  the  right  auricle  lies  behind  the  sternum, 
while  its  lower  two  thirds  are  to  the  right  of  this  bone.  The  left 
auricle  is  situated  behind,  being  completely  invested  by  the  left 
lung  and  entirely  obscured  from  view  from  the  front.  The  same 
is  the  case  also  with  the  left  ventricle,  excepting  a  narrow  strip 
which  forms  the  left  border  of  the  heart  and  is  visible  anteriorly.' 
It  is  the  inferior  extremity  of  this  narrow  strip  which,  propelled 
against  the  wall  of  the  thorax,  occasions  the  apex-beat.  Conse- 
quently it  is  a  portion  of  the  right  ventricle  only  which  is  exposed 
to  view  after  removal  of  the  breastbone  and  adjacent  costal  car- 
tilages. The  remainder  of  the  heart,  even  that  which  lies  ante- 
riorly, is  covered  from  view  by  the  lungs. 

The  anterior  lung  borders  are  in  apposition  behind  the  middle 
of  the  sternum  from  the  level  of  the  second  to  that  of  the  fourth 
costal  cartilages.  At  this  latter  situation  they  diverge,  the  border 
of  the  right  lung  passing  on  downward  to  the  level  of  the  fifth 
right  costal  cartilage,  where  it  turns  off  to  the  right  to  unite  with 
the  inferior  margin  of  the  same  lung.  The  anterior  margin  of 
the  left  lung  diverges  abruptly  at  the  level  of  the  fourth  cartilage, 
passing  outward  along  the  lower  edge  of  this  cartilage  as  far  as  its 
union  with  its  rib.  It  then  turns  downward,  and,  after  curving 
slightly  inward  and  then  outward,  unites  with  the  inferior  border 
at  the  level  of  the  sixth  costal  cartilage  near  its  point  of  articu- 
lation with  its  rib.  In  consequence  of  this  peculiar  arrangement 
of  the  left  lung  a  portion  of  the  anterior  surface  of  the  right  ven- 
tricle comes  into  immediate  contact  with  the  chest-wall,  and,  being 
uncovered  by  lung,  forms  the  area  of  superficial  cardiac  dulness. 
By  many  this  area  is  considered  of  great  importance  in  the  deter- 
mination of  the  size  of  the  heart  by  percussion,  as  will  be  shown 
in  dealing  with  the  subject  of  cardiac  percussion. 

Position  of  the  Great  Vessels  and  Valves. — The  pulmonary 
artery  lies  about  half  an  inch  to  the  left  of  the  breastbone  and 
extends  from  the  level  of  the  centre  of  the  third  left  interspace 
upward  to  the  level  of  the  second  costal  cartilage,  where  it  divides 
into  its  two  main  branches.     The  position  and  course  of  the  as- 


DISEASES  OF  THE  HEART 


cending  aorta  inav  be  represented  by  a  line  drawn  from  the  third 
left  chondro-sternal  articulation  ni)ward  across  the  breastbone  to 
the  junction  of  the  right  edge  of  that  bone  with  the  second  right 
costal  cartilage,  which,  therefore,  is  sometimes  spoken  of  as  the 
aortic  cartilage,  because  at  this  point  the  aortic  valve-sounds  are 
most  distinctly  heard.  The  superior  vena  cava  passes  downward 
along  the  right  cardiac  border  from  the  level  of  the  second  costal 
cartilage  to  a  point  opposite  the  middle  of  the  third  right  inter- 
space. 

The  four  sets  of  valves  are  bunched  closely  together  not  far 
from  the  junction  of  the  third  left  costal  x;artilage  with  the  border 

of  the  sternum,  the  pulmonary 
being  most  superficial,  the  mi- 
tral most  internal,  the  tricuspid 
most  inferior,  and  the  aortic 
the  most  central.  They  cannot, 
-  '^  therefore,  be  auscultated  in  the 
region  of  their  anatomic  seat 
.1  p^if  one  is  to  differentiate  their 
individual  sounds.  For  this 
reason  we  take  advantage  of 
the  laws  governing  the  conduc- 
tion of  their  sounds  and  aus- 
cultate them  in  certain  areas 
named  after  the  respective 
valves. 

Thus  the  mitral  area  is 
situated  at  the  apex-beat  and 
includes  a  limited  district  im- 
mediately roundabout.  The 
tricuspid  area  includes  the  lower  end  of  the  sternum  and  a  portion 
of  the  surrounding  region.  The  pulmonic  area  is  located  in  the 
second  left  intercostal  space  close  to  the  edge  of  the  breastbone, 
while  the  aortic  area  lies  in  the  corresponding  situation  on  the 
opposite  side.  It  must  not  be  supposed  that  the  valve-sounds  and 
murmurs  are  heard  only  in  these  situations — they  are  widely 
propagated  iiiid  blend  witli  one  another,  and  in  particular  endo- 
cardial murmurs  are  often  so  widely  conducted  as  to  he  distinctly 
audible  in  other  areas  than  those  to  which  they  properly  belong. 


Fio.  1.— Cardiac  Valve  Akeas. 
Sounds  produced  at  various  valves  indicated : 
p,  pulmonary  :  a,  aortic ;   <,  tricuspid ;  ^u, 
mitral. 


INTRODUCTORY  5 

Leaving  further  consideration  of  this  subject  at  this  time,  we  now 
pass  on  to  the  discussion  of  the  methods  by  which  the  size  of  the 
heart  is  ascertained  during  life  (Fig,  1). 

Cardiac  Percussion. — In  employing  this  means  of  examination 
we  aim  to  determine,  first,  the  boundaries  of  the  area  of  superficial 
dulness,  and  second,  the  limits  of  deep-seated  dulness.  To  accom- 
plish the  former,  percussion  must  be  made  lightly,  whereas  the 
latter  requires  a  firm,  heavy  percussion-stroke. 

The  area  of  superficial  or  absolute  cardiac  dulness  correspond- 
ing with  the  portion  of  the  right  ventricle  uncovered  by  lung 
during  inspiration,  extends  vertically  from  the  upj)er  edge  of  the 
fourth  left  costal  cartilage  to  the  sixth,  and  transversely  from 
the  left  border  of  the  sternum  to  a  point  midway  between  the 
parasternal  and  mamillary  lines.  As  its  outer  or  left  boundary 
is  irregular,  and,  roughly  speaking,  passes  obliquely  downward 
towards  the  left,  this  area  is  broader  at  its  lower  than  at  its  upper 
margin.  Enlargement  of  the  heart  crowds  the  lung-borders 
aside,  and  hence  generally  increases  the  dimensions  of  superficial 
dulness,  especially  to  the  right  in  cases  of  hypertrophy  and  dila- 
tation of  the  right  ventricle.  But  a  variety  of  conditions  outside 
of  the  heart  may  increase  or  diminish  the  extent  of  superficial 
dulness,  and  hence  render  this  not  always  a  trustworthy  indication 
of  the  actual  size  of  the  heart.  Thus  the  lung-borders  may  be  re- 
tracted by  pleuritic  adhesions  and  expose  an  abnormally  large 
portion  of  the  right  ventricle,  or  being  distended  by  pulmonary 
emphysema,  they  may  diminish  or  entirely  obliterate  this  area. 

Consequently  it  is  preferable  to  rely  upon  deep  rather  than 
superficial  percussion  in  endeavouring  to  ascertain  the  size  of  the 
heart,  since  when  the  limits  of  deep-seated  or  relative  cardiac 
dulness  are  found  increased  we  know  it  is  due  to  increase  in  the 
size  of  the  organ  itself.  Vierordt  objects  to  this  latter  method 
because  of  its  greater  difficulty  and  uncertainty,  since  pulmonary 
resonance  shades  so  gradually  into  the  relative  dulness  overlying 
the  heart  that  two  observers  of  apparently  equal  skill  may  not 
agree  in  their  results.  Doubtless  individual  judgment  depends 
very  largely  upon  practice  and  delicacy  of  hearing,  and  doubtless 
emphysema,  inelasticity  of  the  ribs,  great  thickness  of  the  parietes, 
etc.,  often  make  it  impossible  to  accurately  determine  deep  cardiac 
limits.     ^Nevertheless  the  cases  in  which  relative  dulness  is  possi- 


DISEASES  OF  THE   HEART 


ble  of  detection  are  so  numerous  that  I  prefer  to  rely  upon  it 
rather  than  on  superficial  dulness,  and  always  urge  students  to 
make  use  of  this  method. 

The  Deep  Boundaries  of  the  Heart  (Fig.  2). — It  is  well  known 
that  all  hearts  are  not  of  the  same  size  even  in  health,  the  male 
heart  being  larger  than  the  female,  and  that  of  a  child  relatively 
larger  than  that  of  an  adult.  Moreover,  the  right  auricle  measures 
more  during  diastole  than  during  systole.     Consequently  measure- 


ments cannot  be  given  that  are  invariable. 


Yet  the  following 


figures  taken  from  Yierordt  may  be  stated  as  the  average.     The 

adult  heart  ''  extends  from 
about  8  or  9  centimetres  to  the 
left  of  the  median  line  (apex  of 
the  heart)  to  about  4  or  5  cen- 
timetres to  the  right  of  the 
same,  i.  e.,  about  one  and  a 
half  finger-breadths  to  the  right 
of  the  right  border  of  the  ster- 
num (right  auricle)."  Busse, 
who  employed  Ebstein's  palpa- 
tory percussion,  found  the  left 
l)order  of  the  heart  in  health 
never  passed  outside  the  mam- 
illary line,  while  Ilornkohl 
determined  the  average  in 
adults  to  be  7.3  centimetres 
from  the  left  sternal  margin. 
On  the  right  side  the  heart  ex- 
tended a  variable  distance  beyond  the  sternum,  depending  on 
the  stature  of  the  man,  being  2.0  centimetres  for  one  130  centi- 
metres tall,  and  3.0  centimetres  for  a  male  of  190  centimetres 
in  height.  In  women  those  figures  are  slightly  less,  while  in 
children  the  area  of  the  heart  measures  relatively  more  than  in 
adults.  Tf  the  median  line  is  taken  as  the  landmark  from  which 
to  measure,  Ilondcohrs  figures  must  be  increased  by  1  to  1.5  centi- 
metre, which,  according  to  Ebstein,  is  half  the  M'idth  of  the  ster- 
num. Consecjuently  it  is  found  that  Vierordt's  and  Hornkolil's 
estimates  are  not  so  much  at  variance  as  they  at  first  appear. 

Three  methods  of  percussion  are  in  use,  and  mentioned  in  the 


Fio.  2. — NoKMAL  Deep-seated  Cahdiac 

Dulness. 

PP.  parasternal  line;  MM,  inaniillary  line. 


INTllODUCTORY  T 

order  of  their  popularity  are:  (1)  plessimetric,  (2)  auscultatory, 
(3)  palpatory  percussion.  I  do  not  propose  to  discuss  the  advan- 
tages or  disadvantages  of  employing  a  pleximeter  and  hammer, 
but  merely  to  express  my  very  positive  preference  for  the  use  of 
the  fingers,  for  the  reason  that  thereby  one  is  enabled  to  obtain 
valuable  information  from  the  sense  of  resistance. 

In  ascertaining  the  area  of  absolute  dulness  light  strokes  are 
essential,  while  the  reverse  is  the  case  as  regards  deep-seated  dul- 
ness. Moreover,  in  outlining  the  area  of  relative  dulness  the 
pleximeter  finger  should  be  pressed  firmly  against  the  chest-vi^all, 
to  exclude  so  far  as  possible  the  vibrations  of  the  bony  structures. 
This  is  the  "  ahgeddmpfte  "  percussion  of  the  Germans.  The 
finger  is  placed  firml}^  at  right  angle  to  the  ribs  at  a  point  well 
outside  the  cardiac  area,  and  percussion  is  made  with  considerable 
force  at  ever  decreasing  distances  from  the  sternum  until  a  slight 
rise  in  pitch  and  increase  of  resistance  indicate  that  the  airless 
organ  (the  heart)  has  been  reached. 

In  this  manner  one  is  to  percuss  from  above  downward  along 
the  left  parasternal  line,  beginning  in  the  first  intercostal  space 
and  ceasing  when  the  upper  border  of  the  liver  is  reached.  At 
the  sides,  percussion  is  to  be  performed  first  in  an  oblique  direc- 
tion from  above  downward  and  inward,  and  next  on  a  transverse 
line  from  without  towards  the  centre.  If,  wherever  comparative 
dulness  is  perceived,  a  mark  is  made  with  a  dermographic  pencil, 
these  marks  can  subsequently  be  united,  and  will  then  represent 
the  probable  limits  and  shape  of  deep-seated  cardiac  dulness.  If 
one  prefers  he  can,  instead  of  placing  his  finger  across  the  ribs, 
press  it  strongly  into  the  intercostal  space  parallel  with  the  ribs, 
and  if  his  finger  is  slender  can  thus  convey  his  percussion-strokes 
more  directly  to  the  heart  without  eliciting  so  much  vibration 
from  the  elastic  structures  intervening. 

Sansom  makes  use  of  a  narrow  pleximeter,  which  is  of  such 
small  size  as  to  fit  well  down  into  the  intercostal  space,  and  claims 
remarkably  accurate  results,  more  precise  indeed  than  in  any 
other  way. 

It  may  be  well  to  here  remark  that,  when  in  women  accurate 
percussion  of  the  heart  is  impossible  on  account  of  the  large  size 
of  the  mammae,  fairly  trustworthy  information  concerning  the 
size  of  the  heart  may  be  gained  by  careful  palpation  of  the  apex- 


8 


DISEASES   OF  THE   HEART 


beat.  Since  the  mamillary  line  is  not  a  trustworthy  guide  in 
females,  it  is  better  to  measure  the  site  of  the  apex  impulse  from 
the  mid-sternal  line  or  from  the  mid-clavicular  line,  it  being  in 
the  fifth  interspace,  an  inch  within  the  latter. 

Two  statements  should  also  be  made  regarding  percussion  of 
the  heart  in  children.  In  the  first  place,  the  area  of  superficial 
dulness  is  said  by  Hornkohl  to  be  somewhat  more  extensive  than 
in  adults,  particularly  above,  where  it  is  asserted  to  reach  up  into 
the  thirtl  intercostal  space,  while  its  outer  margin  passes  some- 
what further  beyond  the  left  parasternal  line,  i.  e.,  to  a  point  a  lit- 
tle nearer  the  mamillary  than  the  })arasternal  line.  In  the  sec- 
ond place,  it  is  important  to  bear  in  mind  the  great  elasticity  of 
the  child's  chest,  and  hence  to  percuss  with  far  more  delicacy  than 
is  advisable  in  grown  people.  Otherwise  the  note  of  pulmonary 
resonance  and  the  vibrations  of  underlying  structures  will  assur- 
edly prevent  accurate  and  trustworthy  results.  For  these  reasons 
it  is  far  preferable  to  rely  on  the  other  modes  of  j)ercussion  now 
to  be  described. 


3. — AUSCCLTATOKV    pERCrssluN. 


Auscultatory  or  Stethoscopic  Percussion. — This  is  a  combina- 
tion of  auscultation  Jind  percussion,  and  is  based  on  the  princijtle 
that  when  the  stroke  is  iiiade  over  a  solid  organ  its  note  is  higher, 


INTRODUCTORY 


Fig.  4. — Auscultatory  PEKCusiioN. 


sharper,  and  more  clearly  defined  tlian  when  over  an  air-contain- 
ing organ.  It  is  found,  moreover,  that  there  is  a  distinct  differ- 
ence in  the  character  of  the  note  of  two  viscera  of  similar  struc- 
ture. This  is,  of  course,  the 
same  jDrinciple  that  underlies 
plessimetric  percussion,  but  the 
auscultatory  method  enables 
one  to  appreciate  more  delicate 
shadings  of  tone  and  to  define 
more  precisely  the  deeply  situ- 
ated borders  of  an  organ  or 
solid  thoracic  tumour.  It  even 
enables  one  to  distinguish  be- 
tween the  dulness  of  pleuritic 
or  pericardial  effusion  and  that 
of  a  contiguous  pulmonary  con- 
solidation. 

It  is  practised  in  either  of 
two  ways :  The  examiner  may 
with    one    hand    hold    the    bell 

of  his  binaural  stethoscope  against  the  centre  of  the  cardiac 
area,  while  with  the  tip  of  a  finger  of  the  disengaged  hand  he 
taps  the  chest-wall  lightly  from  without  inward  and  on  a  line 
with  his  stethoscope  (Fig.  3),  or  he  may  have  his  instrument 
held  by  an  assistant  while  he  performs  percussion  in  the  ordi- 
nary manner  (Fig.  4).  The  former  mode  is  preferable,  because 
more  delicate.  Such  astonishing  and  incredible  accuracy  is 
claimed  for  auscultatory  percussion,  notably  by  Bezly  Thorne, 
that  Broadbent  and  others  have  been  led  to  test  it,  and  have  come 
to  the  conclusion  that  it  possesses  no  advantages  over  plessimetric 
percussion.  I  have  employed  it  a  great  deal,  and,  although  recog- 
nising its  liability  to  error  and  its  limitations,  still  I  believe  it  is 
in  certain  cases  with  thin-walled  elastic  chests  and  when  practised 
carefully  a  very  accurate  means  of  outlining  the  heart.  I  have 
repeatedly  compared  its  findings  with  those  of  the  two  other  meth- 
ods, especially  plessimetric,  and  find  it  satisfactory  and  trust- 
worthy. One  occasionally  encounters  chests  in  which  for  one  rea- 
son or  another  it  is  next  to  impossible  to  determine  the  deep  limits 
of  the  heart  in  the  ordinary  fashion.     It  is  well  in  such  cases  to 


10 


DISEASES  OP  THE   HEART 


try  the  method  under  discussion,  since  it  will  often  help  one  out 
of  his  dilemnia.  I  should  not  recommend  its  employment  to  the 
exclusion  of  the  plessimetric  method,  but  merely  as  an  adjunct 
thereto. 

Palpatory  Percussion. — By  this  term  is  meant  a  method  of 
using-  both  palpation  and  percussion  at  the  same  time.  In  other 
words,  it  is  a  method  of  ascertaining  the  heart's  resistance,  and 
thereby  of  ascertaining  its  outline  and  dimensions.  It  makes  use 
of  the  feeling  of  resistance  rather  than  of  the  auditory  ])erception 
of  ditl'ercnces  in  sound.  Auenbruggcr  and  Lacnnec  percussed  the 
chest-wall  immediately — that  is,  without  the  intervention  of  a  ples- 
simeter ;  the  former,  by  striking  with  the  tip  of  his  finger,  and  the 
latter  w^ith  the  end  of  his  stethoscope.  It  is  needless  to  say  this 
mode  of  performing  ])ercussion  is  more  or  less  painful  to  the  pa- 
tient. In  1S77  Ebstein  proposed  pal})ation  of  the  heart  and  other 
solid  viscera,  as  the  liver,  as  a  means  of  appreciating  their  size 
by  their  resistance,  and  at  the  International  Medical  Congress 
at  Rome  in  1S94  he  read  an  elaborate  paper  in  which  he  discussed 

and  explained  his  method  at 
considerable  length.  In  this 
paper  he  called  attention  to  a 
method  employed  by  J.  Ilein, 
which  consists  in  palpating  the 
heart  with  one  finger  while  per- 
cussing with  the  other  in  the 
following  manner:  The  palmar 
surface  of  the  terminal  phalanx 
of  the  outstretched  middle  fin- 
ger is  placed  upon  the  chest, 
wliile  a  light  tap  is  made  on 
the  chest  with  the  tip  of  the  bent 
forefinger  (Figs.  5  and  (!).  Then 
wliilo  the  extremity  of  the  first 
finger  rests  against  the  wall  of 
the  thorax  ho  gives  a  light  blow 
to  the  chest  with  tlie  pad  of  llic  middle  finger.  In  each  instance 
the  fingers  are  allowed  to  rcmaiii  foe  an  iiistaiit  in  contact  with 
the  part  percussed,  so  as  the  better  to  perceive  the  sensation  of 
resistance  imparted.     In  this  way,  by  alternately  tapping  with  the 


b'm.  ;■). — IIein'h  I'Ai.rATuUY   I'kkci  ssmN. 
First  position. 


INTRODUCTORY 


11 


two  fingers,  the  entire  area  is  traversed.  This  is  said  to  yield  very 
accurate  results,  but  is  by  Ebstein  considered  inferior  to  his 
method,  because  not  altogether  devoid  of  pain  to  the  patient. 
Ebstein,  therefore,  makes  use  of  a  small  glass  pleximeter,  upon 
which  he  gives  a  gentle  prejssing 
stroke  with  the  tip  of  one  fin- 
ger, which,  flexed  at  its  meta- 
carpal articulation,  is  held 
slightly  and  rigidly  curved  as 
the  stroke  is  given  (Fig.  7). 
The  blow  is  not  made  with  a 
quick  rebound  (staccato),  but 
with  a  firm  pushing  movement 
(legato).  The  stroke  is  given 
in  a  line  perpendicular  to  the 
surface  thus  percussed  and  the 
pleximeter  is  held  firmly  in 
position.  Ebstein' s  pleximeter 
of  glass  is  ^  an  inch  (1.3  centi- 
metre) in  width.  If  inch  (4.0 
centimetres)  in  length,  and  sur- 
mounted by  a  small  handle  f  of  an  inch  (1.5  centimetre)  in  height. 
With  such  a  pleximeter  Ebstein  asserts  the  method  is  not  only 
gratifyingly  precise,  as  he  has  repeatedly  proved  on  the  cadaver 
by  means  of  needles,  but  is  easily  acquired,  which  is  an  opin- 
ion contrary  to 
that  expressed  by 
Vierordt.  More- 
over, it  possesses 
the  additional 
advantage  of  en- 
abling the  ex- 
aminer to  avail 
himself  of  his 
perception  of  the 
sound  and  pitch 
of  the  note  pro- 
duced, as  well  as  of  the  sense  of  resistance.  In  this  way  two 
impressions  are  received  simultaneously  which  serve  to  control 


Fig.  6.- 


-Hein's  Palpatoby  Percussion. 
Second  position. 


Ebstein's  Palpatory  Percussion. 


12 


DISEASES  OF  THE  HEART 


-.Maolike's  Method  of  Pali-atouy 
Pekclssion. 


each  other.  Ebstein  dechires  also  that  by  his  method  one  can 
obtain  satisfactory  results  in  .cases  of  emphysema  and  in  persons 
with  a  thick  ])annic\ihis  of  fat  or  large  mammary  glands,  all  of 

which  nsually  preclude  accu- 
rate percussion  after  the  ordi- 
nary .method. 

Robert  Maguire,  of  Eng- 
land, advocates  palpator}^  per- 
cussion by  tapping  lightly  with 
the  soft  palmar  cushion  of  the 
terminal  phalanx  of  one  finger, 
and  claims  equally  accurate  re- 
sults (Fig.  S).  lie  expressly 
states  that  the  stroke  must  be 
not  short  and  quick,  but  long 
and  ])ressing,  as  if  one  were 
feeling  or  palpating  with  the 
finger.  It  is  applicable,  he 
says,  not  only  to  all  solid  or- 
gans, spleen  and  kidneys,  as 
well  as  heart  and  liver,  but  also  to  collections  of  fluid  in  thoracic 
and  peritoneal  cavities. 

In  cases  which  are  at  all  obscure  it  is  well  to  verify  the  con- 
clusions derived  by  any  one  method — plessimetric,  auscultatory,  or 
palpatory — by  each  of  the  others.  For  my  part  I  value  the  aus- 
cultatory method  the  least  highly,  because  so  liable  to  error  in 
exactly  those  cases  ^\■llicll  oflVr  the  greatest  difficulty  to  ordinary 
percussion — that  is,  ('iii])]iyscuiatous,  fat,  and  rigid  chests. 

Auscultation  of  the  Heart  is  another  and  indispensable  means 
of  making  cardiac  examinations,  and  by  the  inexperienced  is  apt 
to  be  relied  upon,  if  not  exclusively,  at  least  to  a  degree  out  of  pro- 
portion to  its  inij)()rtance  as  comjiared  with  ])ercussion.  Neither 
can  be  comjiletc  without  the  other.  I  desire  also  to  emphasize  the 
folly  of  iittcinpting  to  do  accurate  work  without  the  use  of  a 
stothoscoj)e.  Whatever  form  or  kind  of  instrument  enables  one 
to  liear  tlu?  most  distinctly  is,  in  my  opinion,  the  best  for  him,  re- 
gardless of  the  arguments  advanced  in  favour  of  certain  sorts.  I 
make;  use  of  a  simple  biiumi-al  and  of  a  inoiiaui'al  stctlioscojx',  em- 
ploying the  laftci-  when  <h'siring  such  information  as  is  sometimes 


INTRODUCTORY  13 

obtained  from  the  iiii])ii]se  of  the  hypertrophied  or  dilated  heart 
against  the  chest-walL  A  stethoscope  with  a  small  end-piece  en- 
ables one  to  difl"erentiate  sounds  and  murmurs  and  to  trace  them 
to  their  source  in  a  way  that  cannot  be  done  by  the  ear  placed 
against  the  pripcordia. 

Normal  Heart-sounds. — The  detection  of  murmurs  is  not  the 
only  object  of  auscultation.  The  heart-sounds  themselves  often 
afford  as  much,  if  indeed  not  more  information  than  do  bruits. 
Therefore,  if  one  is  to  correctly  interpret  what  he  hears  come 
from;  the  heart,  he  must  be  familiar  with  the  characters  of  the  nor- 
mal sounds  of  this  organ.  To  this  end  he  must  know  how  they 
are  produced,*  and  keep  in  mind  what  is  going  on  within,  during 
the  portions  of  the  cardiac  cycle,  at  the  time  of  the  sounds  and 
during  the  intervals  of  silence. 

If  one  listens  at  any  point  upon  the  cardiac  area  he  hears  two 
distinct  sounds,  known  as  the  first  and  second  sound  respectively. 
Over  either  of  the  ventricles,  in  the  neighbourhood  of  the  apex, 
the  accent  falls  on  the  first,  which  is  longer,  of  a  lower  pitch,  and 
more  intense — that  is,  more  booming  than  the  second,  which  is, 
conversely,  short,  sharp,  and  clicking,  having  a  valvular  quality 
we  say.  Moreover,  the  ear  detects  two  intervals  or  periods  of 
silence,  of  which  the  shorter  occurs  during  systole  between  the 
first  and  succeeding  second  sound.  The  longer,  known  as  the 
pause,  falls  between  the  second  and  next  ensuing  first  sound,  dur- 
ing diastole.  This  succession  of  sounds  and  silences  gives  to  the 
heart-sounds  their  peculiar  rhythm,  likened  to  the  ticking  of  a 
clock.  If  now  auscultation  be  made  at  the  base  of  the  organ,  in 
the  second  interspace  at  either  side  of  the  sternum,  it  is  perceived 
that  the  accent  falls  on  the  second  sound,  since  this  is  the  louder 
and  clearer  and  higher  pitched  of  the  two.  Their  rhythm  is,  how- 
ever, the  same  as  at  the  apex.  Furthermore,  it  is  generally  per- 
ceived that  the  second  sound  is  louder  on  one  side  of  the  sternum 

*  It  is  common  to  speak  of  sounds,  whether  normal  or  abnormal,  as  produced 
within  the  heart  or  chest.  Of  course  such  phraseology  is  loose  and  not  in  accord- 
ance with  the  known  laws  of  acoustics.  Sounds  are  the  auditory  perception  of 
waves  imparted  to  the  air  by  the  vibration  of  structures  within  the  thorax,  the 
tissues  serving  as  good  condiictors  of  these  vibrations.  With  this  understanding 
of  the  mode  of  production  of  these  acoustic  phenomena,  I  shall,  for  the  sake  of 
convenience  and  the  avoidance  of  circumlocution,  speak  of  sounds  as  generated 
in  the  heart  or  chest. 


14 


DISEASES  OF  THE  HEART 


tlian  on  the  other,  the  position  of  greater  intensity  not  always 
being  uniform  in  different  individuals,  depending  on  various  con- 
ditions, as  age,  etc. 

What  occasions  this  slight  diversity  between  the  sounds  at 
the  apex  and  base  ?  Why  do  not  the  two  sounds  in  all  situa- 
tions have  the  same  character  ?  I  will  answer  the  latter  query 
first.  The  first  sound  is  synchronous  with  the  apex-beat,  and 
is  therefore  produced  during  ventricular  systole.  Physiology 
teaches  us  that  the  duration  of  this  phase  of  the  cardiac  cycle 
is  .j^  of  a  second,  subdivided  as  follows  (Fig.   9) :  During  the 


Fig.  9. — Normal  Cardiac  Cycle. 
Phases  of  cycle  above  line ;  sounds  below. 

first  tenth  of  a  second  the  ventricle  is  initiating  its  contraction 
and  is  silent;  during  the  following  -^j^  of  a  second  its  contrac- 
tion reaches  its  maximum  energy,  the  auriculo-ventricular  valves 
close,  and  the  first  heart-sound  is  heard ;  the  final  tenth  of  the 
second,  diiring  which  the  ventricle  still  remains  contracted,  is 
again  a  period  of  silence  and  terminates  the  phase  of  ventricular 
systole. 

During  the  stage  of  active  contraction  l)h)od  is  being  forced 
from  the  ventricles  into  the  aorta  and  pulmonary  artery.  With 
the  completion  of  this  propulsive  stage  the  ventricles  relax;  arte- 
rial walls  recoil,  forcing  the  mass  of  blood  against  the  sigmoid 
valves,  which,  thus  thrown  into  tension  and  closed,  give  forth  a 
tone,  the  second  sound,  which  signals  the  closure  of  the  valve  and 


INTRODUCTORY  15 

the  commencement  of  diastole.  This  sound  is,  therefore,  diastolic, 
and,  ushering  in  the  stage  of  cardiac  repose,  is  succeeded  Ly  the 
period  of  silence  or  long  pause. 

This  brief  statement  of  what  takes  place  during  the  different 
phases  of  the  cardiac  cycle  will  help  us  to  understand  the  mode 
of  production  of  the  two  sounds.  During  the  middle  portion  of 
systole,  when  the  first  sound  is  audible,  the  ventricle  is  actively 
contracting  and  the  auriculo-ventricular  valves  are  closed  and  held 
closely  in  contact  through  the  contraction  of  the  papillary  muscles. 
Experiments  have  shown  that  if  either  participant  in  this  stage 
can  be  made  to  act  without  the  other  a  sound  is  still  audible,  but 
it  has  lost  its  normal  character.  If  in  the  bloodless  heart  the  ven- 
tricles are  made  to  contract  while  the  auriculo-ventricular  valves 
are  hooked  back,  the  sound  is  low  in  pitch,  prolonged,  and  boom- 
ing, while  if  the  ventricle  be  opened  and  the  valves  closed  without 
contraction  of  the  muscular  walls,  the  sound  produced  is  higher 
pitched,  shorter,  and  less  intense.  It  is  thus  apparent  that  the 
first  cardiac  sound  is  a  composite  one  made  up  of  two  elements,  a 
muscular  and  a  valvular. 

On  the  other  hand,  the  second  sound  is  due  solely  to  the 
vibrations  generated  in  the  semilunar  valves  at  the  instant  of 
their  closure  and  possesses  no  muscular  element.  It  is  conse- 
quently of  higher  pitch,  shorter  duration,  and  less  intensity  than 
the  first  sound.  Inasmuch  as  the  first  is  a  composite  sound,  it  is 
obvious  that  its  two  elements  must  synchronize  exactly  if  the  sound 
is  to  be  pure  and  normal.  Furthermore,  there  are  two  ventricles 
and  two  sets  of  auriculo-ventricular  valves.  Consequently  each 
half  of  the  heart  is  responsible  for  its  own  first  sound.  Ausculta- 
tion at  the  apex,  however,  reveals  but  one  first  soimd,  which  is  the 
result  largely  of  the  blending  of  the  two  sounds  generated  in  the 
two  halves  of  the  organ,  but  conducted  to  this  point.  That  this  is 
the  case  is  proved  by  the  clinical  experience  that  occasionally  over 
one  or  the  other  ventricle  the  systolic  sound  is  heard  to  be  of 
altered  quality  or  divided  into  its  two  elements,  while  over  the 
opposite  half  of  the  organ  it  retains  its  normal  characters. 

Inasmuch  as  there  are  two  sets  of  semilunar  valves,  there  are 
two  separately  produced  yet  synchronous  second  sounds.  Of  these, 
the  aortic  is  heard  most  distinctly  at  the  right  edge  of  the  sternum 
in  the  second  interspace,  while  the  area  of  greatest  audibility  for 


16  DISEASES   OF   THE    HEART 

thu  pulmonic  is  in  tlic  forrespoii(liiig  interspace  at  tlie  left 
border  of  the  sternnni.  Jn  the  early  years  of  life,  by  some  said 
to  be  up  to  the  thirtieth,  the  pulmonic  second  sound  is  the 
louder  of  the  two,  while  at  and  after  middle  age  the  reverse 
obtains. 

Conditions  which  raise  blood-i)ressure  in  either  the  lesser  or 
greater  system  will  correspondingly  alter  the  intensity  of  these 
sounds.  The  more  feeble  iirst  sound  heard  at  the  base  at  either 
sternal  margin  is  probably  transmitted  thither  from  the  respective 
ventricle.  Tiegerstedt  says  it  is  not  impossible  that  vibrations 
caused  by  the  o])ening  of  the  semilunar  valves  play  a  certain  role 
in  the  production  of  the  first  heart-sound.  If  this  be  the  case,  then 
the  systolic  tone  audible  at  the  base  of  the  heart  in  the  aortic  and 
pulmonary  areas  respectively,  is  not  to  be  regarded  merely  as  a 
conducted  sound  transmitted  thither  with  less  intensity  than  to 
the  apex. 

Reduplication  uf  the  IleaH-sounds. — Either  the  first  or  second 
sound  may  under  certain  conditions  be  doubled — that  is,  divided 
into  two  parts  or  split,  as  is  sometimes  said.  This  occurs  most  fre- 
quently with  the  second  sound,  and  is  best  heard  over  the  base  of 
the  heart.  It  may  be  iiei'ceived  if  the  breath  is  held  at  the  close 
of  a  deep  ins])iration,  and  under  these  circumstances  is  spoken 
of  as  physiological.  Falhologically  such  a  reduplication  is  appar- 
ent when  in  consequence  of  disease  there  is  an  alteration  of  blood- 
pressure  in  either  the  pulmonic  or  aortic  system.  It  is  most  fre- 
quently observed  in  mitral  or  pulmonary  diseases  which  augment 
blood-pressure  in  the  vessels  of  the  lesser  circulation.  It  has  been 
contended  that  in  such  a  condition  the  valves  at  the  ])uhii(tnic  oi'i- 
fice  close  slightly  earlier  than  do  the  aortic  curtains,  and  emit 
their  sound  an  ap])r('ciable  interval  of  time  in  advance.  0})})o- 
nents  of  this  theory  achiiit  the  lack  of  synchronism  in  the  closure 
of  the  two  sets  of  sigmoid  valves,  but  maintain  that  the  increase 
in  blood-pressure  causes  a  delay,  not  a  premature  occurrence  of  the 
sound,  since  to  overcome  the  unnatural  resistance  in  the  pulmonary 
artery  tlic  ventricle  is  comix'lhMl  to  contract  more  slowly  (Barr). 
Jn  other  words,  the  ventricle,  whether  right  or  left,  de])ending  on 
the  sy.stem  in  which  blood-jiressui'e  is  raised,  ('om))letes  its  systole 
perceptibly  latci'  tlian  does  its  fellow.  (Jnttnuniirs  theory  of  the 
doubling  of  the  souiul   being  due  to  asyuclii-oiious  closure  of  the 


INTRODUCTORY  lY 

individual  leaflets  of  a  valve  is  regarded  as  fallacious.  Reduplica- 
tion of  the  second  sound,  therefore,  is  an  indication  of  some  alter- 
ation of  blood-pressure  in  one  or  the  other  system. 

There  is  another  form  of  doubling  of  the  second  sound  which, 
among  English  writers,  who  appear  to  have  paid  particular  atten- 
tion to  this  anomaly  of  the  heart-sounds,  is  distinguished  from  the 
foregoing  as  apparent  or  simulated  douhling.  This  variety,  if  I 
may  so  term  it,  is  heard  only  at  or  near  the  apex,  and  appears  to 
be  confined  to  cases  of  mitral  disease  with  predominating  stenosis. 
The  phenomenon  is  believed  to  be  due  to  the  addition  or  inter- 
polation of  a  third  sound  closely  following  the  physiological  second. 
The  only  theory  regarding  its  mode  of  production  that  appears 
tenable  is,  so  far  as  I  am  able  to  learn,  that  advanced  by  Sansom. 
He  believes  it  to  be  a  sound  of  tension  in  the  altered  segments  of 
the  mitral  valve.  Upon  the  occurrence  of  ventricular  diastole  the 
mass  of  blood  held  back  during  systole  in  the  left  auricle  and 
pulmonary  veins  rushes  forcibly  into  the  rapidly  relaxed  ventricle, 
and,  streaming  in  the  direction  of  least  resistance,  fills  the  space 
behind  the  thickened  and  displaced  mitral  cusps,  "  bellying  them 
out,"  after  the  manner  of  sails  filled  by  the  wind.  This  sudden 
bulging  of  the  diseased  curtains  produces  a  sound  of  tension  which 
is  audible  in  the  fore  part  of  diastole  soon  after  the  normal  second 
sound,  which  in  mitral  stenosis,  in  Sansom's  opinion,  is  the  2^ul- 
monic  second,  transmitted  to  the  apex.  The  aortic  second  is,  he 
thinks,  too  feeble  to  be  heard  at  the  apex.  That  this  third  ele- 
ment of  sound  is  produced  at  the  mitral  orifice  seems  supported 
by  the  observation  that  it  occasionally  becomes  transformed  into 
a  diastolic  murmur  occupying  the  same  position  in  diastole — i.  e., 
following  the  normal  second  sound.  The  diagnostic  value  of  this 
seeming  doubling  of  the  second  sound  at  the  apex  will  be  discussed 
in  the  chapter  on  Mitral  Stenosis. 

Sewall  likewise  attributes  this  reduplication  of  the  second 
sound  to  the  tone  of  valve-tension,  but  explains  it  on  the  hypothesis 
that  the  irritable  papillary  muscles,  stimulated  by  the  inrush  of 
blood  from  the  overdistended  auricle,  contract  too  soon — i.  e.,  in 
the  fore  part  of  diastole.  This  explanation  may  hold  for  those 
cases  in  which  doubling  of  the  second  sound  is  a  transient  phe- 
nomenon, as  heard  sometimes  during  states  of  great  cardiac  ex- 
citement, but  not  for  cases  of  mitral  stenosis. 


18  DISEASES  OF  THE   HEART 

Reduplication  of  the  First  Sound. — Under  certain  conditions, 
as  that  of  abnormal  blood-pressure  within  one  or  the  other  ventricle, 
there  is  heard  not  a  single  first  sound,  but  a  reduplication  or  split- 
ting of  this  sound.  This  abnormality  is  less  frequently  perceived 
than  is  doubling  of  the  second  sound,  and  is  equally  difficult  of 
satisfactory  explanation.  Two  main  theories  are  advanced  to  ac- 
count for  it.  One  of  these  finds  its  causation  in  a  hemisystole,  by 
which  is  meant  the  separate  and  independent  contraction  of  the 
two  ventricles.  Although  there  have  been  recorded  a  few  cases  in 
which  highly  competent  and  careful  observers  believed  they  de- 
tected such  hemisystole,  still  it  is  so  at  variance  with  the  physiol- 
ogy of  the  cardiac  action  to  suppose  the  ventricles  can  fail  to  syn- 
chronize in  their  systoles  that  many  authors  are  not  willing  to 
accept  this  explanation.  The  other  theory  assumes  that  the  two 
components  of  the  first  sound  in  one  or  the  other  side  of  the  heart 
do  not  fall  together,  but  are  separated  by  a  brief  yet  distinct  in- 
terval of  time,  so  that  to  the  ear  the  first  sound  over  that  ventricle 
gives  the  impression  of  splitting  or  reduplication.  One  or  the 
other  constituent  of  the  sound  is  generated  either  too  soon  or  too 
late  to  synchronize  with  the  other.  As  the  phenomenon  occurs 
when  blood-pressure  in  one  of  the  ventricles  is  too  high,  and  as 
under  these  conditions  the  cardiac  wall  has  lost  its  normal  tonicity, 
it  seems  reasonable  that  the  tension  into  which  the  valves  are 
thrown  and  the  contraction  of  the  heart-wall  should  not  be  per- 
fectly simultaneous.  Sewall  argues  that  the  cause  of  the  redupli- 
cation lies  in  the  failure  of  the  papillary  muscles  to  contract  at 
their  proper  time,  their  contraction,  and  hence  the  note  of  valve- 
tension,  occurring  either  before  or  after  that  of  the  ventricular 
wall.  Whatever  l)e  the  true  explanation  of  this  phenomenon,  its 
occurrence  betokens  excessive,  and  it  may  be  dangerous,  increase 
of  pressure  in  that  ventricle,  to  which  the  reduplication  can  be 
traced.  It  may  be  audible  over  either  half,  and  I  recall  a  case  of 
mitral  regurgitation  in  which  this  doubling  appeared  in  the  right 
ventricle  only  when  the  patient  assumed  the  recundK'nt  ])()stiire. 
It  is  not  sehhtiii  present  over  the  left  ventricle  in  cases  of  chronic 
nephritis,  and  then  betokens  (hingerous  excess  of  blood-pressure 
in  tlu!  arterial  system,  and,  secondarily,  within  the  left  ventricle. 

Gallop  or  Canter  Rhythm. — A  ithciioiiienon,  sometimes  ob- 
served and  due  to  the  interpolation  of  a  third  sound   (which,  ac- 


INTRODUCTORY  19 

cording  to  its  position  in  the  diastole,  produces  an  apparent  redu- 
plication of  either  the  first  or  second  sound),  resembles  so  closely 
the  hoof-beats  of  a  galloping  horse  that  it  has  been  termed  the 
canter-rhythm  or  bruit  de  galop.  The  merit  of  having  first  de- 
scribed it  is  accorded  by  the  French  to  Bouillaud ;  yet  to  Potain, 
but  to  Barie  in  particular,  belongs  the  credit  of  having  first  brought 
it  to  the  notice  of  the  profession.  Fraentzel  has  also  given  a  most 
clear  and  discerning  description  of  the  phenomenon  based  on  accu- 
rate scientific  observation.  When  the  peculiarity  under  considera- 
tion is  present,  the  auscultator  hears  not  merely  two  sounds  of 
normal  relative  strength  and  rhythm,  but  three,  of  which  the  last 
is  an  accidental  or  interpolated  sound  occurring  in  the  long  pause. 
Frangois-Franck,  according  to  Sewall,  is  authority  for  the  state- 
ment that  this  third  sound  may  occur  in  any  one  of  three  posi- 
tions :  Immediately  after  the  normal  second,  in  the  middle  of  the 
diastolic  interval,  or  at  the  end  of  the  long  silence  shortly  before 
the  first  sound.  When  it  falls  directly  after  the  normal  second 
sound,  it  must  not  be  confounded  with  the  apparent  doubling  of 
the  second  sound  already  described.  It  is  distinguishable  from 
this  latter  by  its  peculiar  tempo.  Its  canter  rhythm  is  imparted  to 
it  by  the  shortening  up  of  the  long  interval. and  by  the  accent  fall- 
ing on  the  middle  one  of  the  three  sounds — i.  e.,  the  normal  second 
(Fraentzel).  If  one  will  imitate  the  sound  of  a  slow  canter  by 
striking  his  hands  on  his  knees,  he  will  at  once  appreciate  the  cor- 
rectness of  Fraentzel's  statement. 

Any  one,  however,  who  has  studied  this  rhythm  of  the  heart- 
sounds  in  a  large  number  of  cases  will  have  appreciated  the  fact 
that  it  not  infrequently  possesses  the  characters  of  a  rapid  gallop 
rather  than  a  slow  canter.  When  such  is  the  case,  Fraentzel's 
description  does  not  apply.  The  tempo  and  accent  are  now 
changed,  as  may  be  proved  by  again  imitating  the  sound  by  the 
hands.  It  will  now  be  observed  that  the  interval  separating  the 
first  from  the  second  sound  is  shorter  than  that  separating  the 
second  from  the  third  or  interpolated  sound,  while  the  accent  falls 
most  sharply  sometimes  on  the  first,  sometimes  on  the  third,  but 
in  every  case  least  strongly  on  the  middle  one  of  the  three  sounds. 
In  still  other  instances  the  rhythm  described  by  Fraentzel  is  main- 
tained, but  the  accent  is  on  the  first  sound,  thus  producing  a  not 
quite  typical  canter-rhythm.      It  is  this  lack   of  uniformity   in 


20  DISEASES  OP  THE   HEART 

i-li_vtlnn  ami  accent,  Avliich,  as  it  sccnis  to  me,  exjilains  the  divcrsit}' 
of  opinion  expressed  bv  different  writers. 

Potain's  explanation  of  the  i)henomenon  is  that  it  is  dne  to  an 
increase  in  the  elastic  resistance  of  the  ventricnlar  wall  over  its 
muscular  tonicity,  in  conseipience  of  which  the  inrush  of  blood 
from  the  auricle  causes  it  to  generate  a  sound  of  tension.  Sewall, 
on  the  other  hand,  attributes  it  to  the  contraction  of  the  papillary 
muscles  taking  place  prematurely — i.  e.,  during  diastole.  What- 
ever be  its  mode  of  production,  this  rhythm  is  an  evidence  of 
abnormal  blood-pressure  within  the  ventricle,  and  hence  of  dan- 
gerous tension  of  its  wall.  Its  occurrence  is  most'  commonly  ob- 
served over  the  left  ventricle  in  cases  of  chronic  nephritis,  par- 
ticularly the  interstitial  variety,  and  when  thus  observed  it  is  to 
be  regarded  as  an  evil  prognostic  omen.  It  indicates  a  giving  way 
of  the  ventricle,  which  is  no  longer  able  to  cope  successfully  with 
the  resistance  in  the  arterial  system. 

I  agree  fully  with  those  who  look  upon  it  as  a  sign  of  the  end 
being  not  far  distant  in  cases  of  chronic  nephritis,  since  I  have 
never  know^n  an  individual  to  recover  in  whom  this  rhythm  was 
detected.  In  the  spring  of  15)00  I  had  under  treatment  a  com- 
paratively young  man,  with  stiffened  arteries  and  interstitial 
nephritis,  who  presented  this  phenomenon  at  different  times  in  its 
most  typical  form.  Several  times,  under  the  influence  of  nitro- 
glycerin and  cathartics,  his  gallop-rhythm  disappeared  entirely, 
becoming  replaced  by  tw'o  heart-sounds  of  normal  rhythm.  Yet 
so  soon  as  pulse-tension  was  increased,  either  through  lessened 
vigour  of  this  medication  or  the  administration  of  digitalis,  the 
ominous  disturbance  of  rhythm  rea])peared.  This  ])atient  suc- 
cumbed after  about  two  months. 

This  interesting  canter-rhythm  is  never  heard  at  the  base  of 
the  heart,  but  always  over  one  or  the  other  ventricle,  and  conse- 
quently in  either  the  mitral  or  tricuspid  area.  It  may  be  of  tran- 
sient duration,  yet  is  often  persistent.  It  may  be  heard  in  hyper- 
tro])liy  alone  or  coud)incd  with  dilatation,  it  may  occur  in  dilata- 
tion alone,  in  acute  infectious  diseases,  such  as  typhoid  fever  and 
di])htheria,  croupous  pneumonia,  scarlatinp,  acute  articular  rheu- 
matism, and  acute  miliary  tuberculosis  (Fraentzel),  all  of  which 
lead  to  myocarditis  or  to  simple  weakness  of  the  heart-walls.  And 
lastly,  it  niay  be  hcai'd  in  jxTiiicions  anirniia,  Icncn'iiiia,  and  grav<> 


INTRODUCTORY  21 

eachexiaj,  which  induce  profound  cardiac  asthenia  and  consequent 
want  of  tonicity. 

According  to  French  authors,  it  sometimes  occurs  over  the 
riglit  ventricle  in  cases  of  gastric  disease,  and  Johnson  says  it  may 
be  produced  by  puhnonary  emphysema.  Fraentzel  mentions  it  as 
occurring  in  other  hmg  affections,  leading  to  dilatation  and  hyper- 
trophy of  this  right  chamber,  with  marked  cachexia.  I  once  ob- 
served a  true  gallop-rhythm  in  the  fourth  and  fifth  right  inter- 
spaces close  to  the  sternum,  for  a  brief  time,  during  which  there 
was  very  obvious  overdistention  of  the  right  cavities  secondary 
to  a  rheumatic  mitral  regurgitation.  The  very  unusual  situation 
of  the  rhythm  in  this  instance  is  only  explicable  by  the  supposi- 
tion that  in  consequence  of  the  enormous  distention  of  the  right 
ventricle  the  auriculo-ventricular  sseptum  had  become  pushed  so 
far  towards  the  right  that  the  wall  of  the  ventricle  extended  to 
the  fourth  and  fifth  right  interspaces.  It  disappeared  so  soon  as 
treatment  had  unloaded  the  cardiac  chambers. 

Murmurs. — This  is  a  comprehensive  term,  which  includes  all 
those  adventitious  acoustic  phenomena  connected  in  some  way 
with  the  heart's  action  and  not  resembling  in  tone  the  normal  car- 
diac sounds.  They  may  be  primarily  divided  into  endocardial  and 
exocardial.  The  endocardial  are  subdivided  into  organic  or  struc- 
tural and  inorganic  or  accidental,  called  also  functional,  anaemic, 
hiemic,  and  dynamic.  Exocardial  are  divisible  into  pericardial, 
pleuropericardial,  and  cardio-pulmonary. 

By  organic  murmurs  are  meant  such  as  owe  their  origin  for 
the  most  part  to  structural  defect  or  alteration  of  the  cardiac  ori- 
fices or  valves — in  other  words,  to  definite  pathological  changes  of 
the  structures  recognisable  after  death.  Accidental  murmurs  can- 
not, on  the  other  hand,  be  ascribed  to  definite  pathological  lesions, 
and  therefore  have  received  a  variety  of  appellations  in  accord- 
ance with  the  various  theories  offered  in  explanation  of  the  phe- 
nomena. 

Endocardial  Murmurs  of  Organic  Origin. — Tliese  were  once 
thought  to  be  caused  by  friction  of  the  blood  in  its  passage  over 
the  roughened  inner  surface  of  the  heart.  This  theory  was  shown 
to  be  untenable  as  long  ago  as  1847,  when  it  was  replaced  by  the 
one  now  generally  accepted — namely,  that  currents  or  eddies  are 
produced  in  the  stream  of  blood,  the  same  as  in  any  other  fluid, 


22  DISEASES  OP  THE  HEART 

whenever  it  passes  a  point  of  constriction  in  its  channel  or  flows 
suddenly  into  a  portion  of  the  containing-tube,  Avhicli  is  wider 
than  that  directly  above.  These  eddies  and  currents  in  their  turn 
generate  vibrations  which  are  audible.  These  secondary  currents 
are  the  fluid  veins  first  demonstrated  by  Savart,  but  applied  by 
Chauveau  to  the  explanation  of  vascular  and  cardiac  murmurs. 

Some  of  the  conditions  governing  their  production  in  the  vas- 
cular system  are  the  following :  Constriction  of  the  coats  of  a  ves- 
sel by  external  pressure ;  projection  into  its  lumen  of  calcareous 
plates  or  masses  capable  of  turning  the  blood-stream  from  its 
direct  course ;  aneurysmal  sacs  or  vascular  dilatations  into  which 
the  blood-stream  may  swirl ;  and  in  the  heart  itself,  all  pathological 
changes  by  which  orifices  are  narrowed  and  valves  rendered  in- 
competent. In  addition,  murnmrs  can  be  produced  by  vibration 
of  thin  membranes  and  bands  as  the  l)lood-current  sweeps  over 
them. 

In  Virchow's  Archives,  Band  cxl,  is  one  of  a  series  of  sug- 
gestive papers,  by  Kichard  Geigel,  wherein  he  takes  exception  to 
the  prevailing  notion  concerning  the  causation  of  endocardial  and 
vascular  bruits.  By  a  series  of  nuithematical  formula'  Geigel  en- 
deavours to  prove  that  if  murmurs  of  tlie  })itch  of  those  usually 
heard  were  produced  by  vibrations  in  the  blood-stream  these  would 
have  to  be  of  a  length  that  would  be  physically  impossible  within 
the  cardiac  cavities.  He  therefore  states  tliat  the  origin  of  bruits 
in  eddies  and  currents  is  utterly  impossible,  and  declares  them  due 
to  transverse  vibrations  of  the  walls  of  the  structures  inclosing 
the  blood-stream.  His  line  of  reasoning  is  ingenious,  and  to  my 
mind  has  much  to  commend  it,  since  the  generally  accepted  theory 
is  not  altogether  satisfactory. 

It  is  this  consideration  which  makes  me  venture  to  dwell  for  a 
few  numients  on  tlic  ex])hinatiou  of  murmurs  ofi^ered  by  David- 
son, of  Edinljurgh.  According  to  liis  tlicory,  murmurs  are  due  to 
vibrations  set  up  in  the  valves  by  the  impact  of  the  blood-stream 
at  an  oblique  angle.  By  niuuerous  experiments  he  claims  to  have 
demonstrated  that  when  a  stream  of  fluid  was  injected  into  a 
rubber  balloon  or  a  portion  of  the  small  intestine,  one  end  of  which 
was  tied  securely  a})out  the  nozzle  of  tlic  syringe  while  the  other 
was  tightly  ligatured,  tlu;  fluid  veins  and  eddies  thus  generated 
at  the  end  of  the  nozzle  witliin  tlie  elastic  receptacle  did  not  pro- 


INTRODUCTORY  23 

(luce  more  than  a  very  faint  murmur,  audible  by  means  of  a  binau- 
ral stethoscope.  When,  however,  the  fluid  was  made  to  strike  the 
inner  surface  obliquely  a  distinct  clear  sound  was  generated,  the 
intensity  of  which  depended  upon  the  force  of  impact.  By  re- 
ducing the  rapidity  and  force  of  the  stream  Davidson  was  able  to 
produce  murmurs  of  varying  loudness  and  roughness.  By  another 
set  of  experiments  he  was  able  in  the  same  manner  to  generate  an 
aortic  systolic  bruit. 

The  conditions  which  favour  the  generation  of  organic  vas- 
cular and  cardiac  murmurs  are  multiform,  and  hence  such  adven- 
titious sounds  vary  in  respect  to  intensity,  pitch,  quality,  and 
duration.  They  also  obey  the  laws  of  conduction  and  are  propa- 
gated in  different  directions,  according  to  the  seat  and  time  of 
their  production.  Moreover,  two  murmurs  of  independent  rhythm 
may  be  generated  at  the  same  orifice,  or  two  or  more  may  be  pro- 
duced simultaneously  at  different  locations.  So  that  if  one  is  to 
differentiate  endocardial  murmurs,  and  correctly  interpret  their 
significance,  he  must  be  familiar  with  these  various  character- 
istics. 

The  intensity  of  a  murmur  bears  a  direct  ratio  to  the  ampli- 
tude of  vibrations  in  the  blood-stream,  and  therefore  to  the  force 
of  cardiac  contractions,  and  is  not  at  all  a  criterion  of  the  gravity 
of  a  lesion.  The  forcible  escape  of  blood  through  a  small  fenes- 
tration in  a  valve-segment,  in  itself  a  comparatively  trifling  regur- 
gitation, may  be  declared  by  a  very  loud  murmur  that  is  audible 
to  the  patient,  or  even  to  a  bystander  a  number  of  feet  distant. 
Thus  Miller  and  Gibbs  narrate  the  instance  of  a  girl  who  pre- 
sented a  murmur  of  such  intensity  that  it  could  be  plainly  heard 
12  feet  away  when  the  listener  was  in  the  same  room  and  patient 
fully  dressed,  and  3  feet  distant  when  separated  from  the  patient 
by  a  closed  door.  On  the  other  hand,  a  very  grave  valvular 
affection  may,  if  cardiac  power  is  feeble,  occasion  a  scarcely  audi- 
ble murmur  or  even  none  at  all.  It  is  well  known,  for  example, 
that  a  presystolic  murmur  of  mitral  stenosis,  intense  while  the 
heart  is  strong,  may  fade  away  to  complete  inaudibility  when  the 
heart  becomes  feeble. 

Conversely,  a  murmur  scarcely  audible  during  a  period  of  car- 
diac asthenia  may  grow  in  intensity  as  heart-power  is  regained. 
This  is  the  case  particularly  in  aortic  regurgitation.     In  the  ex- 


24  DISEASES   OP   THE   HEART 

aniiiiation  of  a  patient  \vc  therefore  avail  ourselves  of  the  knowl- 
edge that  forcible  cardiac  action  intensiiies  a  luurniur  l)v  having 
him  jnnip  about  or  otherwise  excite  his  heart  to  bring  out  an 
otherwise  faint  or  inaudible  murmur. 

Posture  also  influences  the  loudness  of  these  sounds,  some 
being  more  plainly,  others  less  distinctly,  heard  in  the  recumbent 
position.  Those  of  stenosis  are  more  intense  in  the  erect  posture, 
while  those  of  regurgitation  are  so  in  the  recumbent.  The  reasons 
for  such  variations  in  intensity  are  based  on  the  influence  of  the 
force  of  gravity,  which  is  greater  in  some  than  in  other  positions 
(Gibson).  Mitral  systolic  murmurs  are  nevertheless  often  louder 
in  the  upright  than  the  supine  posture,  an  effect  to  be  attributed 
to  the  greater  vigour  of  ventricular  contraction  when  the  patient 
stands.  There  are  so  many  exceptions  to  the  effect  ordinarily 
exerted  by  position  that  a  patient  should  always  be  examined 
sitting,  standing,  and  reclining. 

The  pitch  depends  upon  the  rapidity  of  the  vibrations  pro- 
ducing the  murmur.  Therefore,  some  murmurs  are  low-])itched, 
while  others  are  high.  The  union  of  overtones  with  the  funda- 
mental tone  determines  quality,  and  as  pitch  and  quality  go  hand 
in  hand,  low-pitched  murmurs  are  apt  to  be  rumbling,  growling, 
rasping,  etc.,  while  shrill  ones  are  often  musical,  whistling,  filing, 
sawing,  twanging,  and  the  like. 

Finally,  the  duration  of  murmurs  is  variable,  depending  on  the 
length  of  time  the  vibrations  endure.  Other  things  being  equal, 
it  requires  more  time  for  the  blood-stream  to  pass  through  a  nar- 
rowed orifice  than  it  does  for  it  to  regurgitate  tlirough  wider  os- 
tium whose  valve  is  defective,  and  therefore  direct  murmurs,  as 
those  of  stenosis  are  called,  are  generally  of  greater  duration 
than  are  the  indirect  ones  of  valvular  insufiiciency.  Tt  may  be 
stated  as  a  general  proposition,  therefore,  that  the  murmurs  of  ob- 
struction are  less  intense,  lower  in  pitch,  less  musical  in  (juality, 
and  of  longer  duration  than  are  those  of  regurgitation,  which, 
for  the  sake  of  emphasis,  may  be  conversely  stated  to  be  higher, 
louder,  more  musical,  and  shorter.  There  are,  however,  excep- 
tions to  this  law.  Fortunately,  murmurs  generated  synchronously 
yet  at  different  ostia  are  never  identical  in  these  four  character- 
istics, and  hence  are  usually  distinguishable  fi-oui  ciK-h  other. 

It  is  also  of  the  utmost  importance  to  note  the  rhythra  of  mur- 


INTRODUCTORY 


25 


murs,  since  in  this  way  alone  can  be  determined  in  what  period 
of  the  cardiac  cycle  they  are  produced.  They  are  either  systolic 
or  diastolic.  Even  the  murmur  of  mitral  and  tricuspid  stenosis 
is  diastolic,  since  it  occurs  during  the  pause ;  yet,  as  it  is  generated 
at  the  time  of  auricular  contraction — that  is,  immediately  prior 
to  ventricular  systole — it  is  commonly  designated  as  presystolic, 
or,  as  proposed  by  Gairdner,  as  auricular  systolic. 

The  transmission  of  a  murmur  is  along  the  surrounding  solid 
media,  and  in  the  general  direction  in  which  the  stream  producing 
it  flows.  It  is  also  governed  largely  by  the  intensity  of  the  mur- 
mur. Fortunately  for  diagnosis,  it  is  this  law  of  conduction  which 
aids  in  the  tracing  of  a  murmur  to  its  seat  of  production.  As 
already  stated,  the  anatomical  locations  of  the  four  orifices  with 
their  valves  are  so  closely  related  within  a  circumscribed  area  that 
if  the  sounds,  of  whatever  nature,  were  not  propagated  to  certain 
regions  where  they  can  be  heard  with  maximum  intensity,  their 
correct  interpretation  would  be  vastly  more  difficult.  Every  exam- 
iner of  experience  has  realized 
the  truth  of  this  in  the  not  very 
infrequent  cases  in  which  mur- 
murs are  widely  conducted  and 
yet  not  most  distinct  in  their 
own  areas. 

Cardiac  Areas. — These  are 
four  in  number,  corresponding 
to  the  ostia,  and  are  definitely 
located  in  circumscribed  regions 
on  the  chest-wall,  where  the  re- 
spective valve-sounds  and  mur- 
murs are  heard  most  clearly 
(Fig.  10).  Thus  the  aortic  area 
is  located  at  the  junction  of  the 

second  right  interspace  and  cor-  Fig.  lO.— Cardiac  Valve  Areas. 

responding  costal  cartilage  with  Sounds  produced  at  various  valves  indicated  : 
, ,       1        T  c  ,  1  ,  rrn  P^  pulmonary :  a,  aortic ;  /,  tricuspid ;  m, 

the  border  oi  the  sternum,     ihe        mitral. 
sounds,     whether     normal     or 

adventitious,  which  are  here  the  loudest,   are  generated   at  the 
aortic  opening.     The  pulmonary  area  lies  in  the  corresponding 
situation  at  the  opposite  or  left  edge  of  the  breastbone.     The 
4 


20  DISEASES  OF  THE   HEART 

pulmonic  sounds  and  nmrniiirs  are  heard  with  maximnni  intensity 
in  this  area,  although  other  bruits  may  be  transmitted  thither  more 
often  perhaps  than  to  the  aortic.  The  tricuspid  area  is  located  at 
the  lower  end  of  the  sternum  and  corresponds  quite  accurately  to 
the  anatomic  seat  of  the  right  auriculo-ventricular  orifice — i.  e., 
between  the  fourth  left  chondro-sternal  articulation  and  the  junc- 
tion of  the  fifth  right  costal  cartilage  with  the  sternum.  Aortic^ 
diastolic,  and  mitral  systolic  murmurs  are  frequently  very  distinct 
in  this  area,  while  tricuspid  bruits  may  often  have  their  greatest 
intensity  at  a  short  distance  therefrom,  at  either  side  or  below. 
The  mitral  area  is  located  at  the  situation  of  the  apex-beat,  but  is 
not  confined  to  this.  Aortic  regurgitant  bruits  are  often  trans- 
mitted, though  feebly,  into  this  region,  and  mitral  systolic  mur- 
murs are  sometimes  even  more  audible  at  some  point  above 
and  to  the  inner  or  outer  side  of  the  nipple  than  directly  at 
the  apex.  Details  regarding  the  conduction  of  the  various  mur- 
murs may  be  found  in  the  respective  chapters  on  valvular  affec- 
tions. 

Before  leaving  the  subject  of  organic  murmurs,  although  still 
more  applicable  to  accidental  ones  about  to  be  considered,  I  wish 
to  caution  against  the  error  of  relying  upon  these  abnormal  sounds 
in  the  diagnosis  of  heart-disease  to  the  exclusion  or  subordination 
of  other  physical  signs.  In  a  sense,  murmurs  are  only  guide- 
posts  which  point  out  the  way  one  is  to  look.  They  are  highly 
valuable  signs,  but  the  information  they  furnish  should  be  con- 
firmed by  secondary  physical  signs,  if  it  is  to  be  taken  to  indicate 
valvular  disease.  A  murmur  may  mislead  one  because  accidental, 
and  the  failure  to  hear  a  bruit  may  do  the  same,  but  secondary 
signs  will  not,  because  they  are  founded  on  changes  in  the  heart 
and  circulation  brought  abo\it  l)y  the  valvular  defect.  The  reader 
will  find  more  on  this  topic  in  the  section  devoted  to  valvular 
lesions. 

Accidental  Murim/rs. — These  are  adventitious  sounds  heard  in 
cardiac  neuroses  and  certain  blood-states,  as  chlorosis  and  various 
forms  of  anfcmia. 

Numerous  terms  are  employed  to  designate  this  class  of  mur- 
murs, as  functional,  inorganic,  hiiemic,  anaemic,  spanajmic,  and 
dynamic.  The  first  two  imply  that  there  is  no  structural  cardiac 
affection,  and  that  the  murmurs  are  in  some  way  dependent  upon 


INTRODUCTORY  27 

perversion  of  the  heart's  function.  ILcmic,  anipmic,  and  spanse- 
mic  connnit  one  to  the  proposition  of  an  altered  blood-state  being 
responsible  for  the  murnmrs.  The  appellation  dynamic  carries 
with  it  the  assmnption  that  the  acoustic  phenomena  depend  upon 
vibrations  set  up  by  powerful,  perhaps  irregular  and  faulty,  action 
of  the  heart-muscle.  The  term  accidental  sufficiently  declares  its 
own  meaning,  and  implies  nothing  more  than  that  the  murmur  is 
a  chance  result  of  cardiac  action. 

Theories  to  account  for  these  murmurs  are  many  and  various, 
and  so  long  as  the  condition  or  conditions  governing  their  produc- 
tion are  not  definitely  ascertained  there  can  be  no  term  that  is 
not  open  to  objection.  These  abnormal  sounds  may  be  heard  in 
any  situation  over  the  organ,  but  are  most  frequent  in  the  pul- 
monic and  mitral  areas.  They  are  systolic  and  have  a  blowing  or 
bellows-like  character.  Such  competent  and  intelligent  observers 
have  advanced  diverse  theories  in  explanation  of  these  murmurs 
that  it  seems  to  me  the  part  of  wisdom  to  assume  that  no  one 
hypothesis  is  applicable  to  all  cases.  May  they  not  have  their 
origin  in  a  variety  of  conditions,  some  within  and  some  without 
the  heart  ?  I  shall  describe  briefly  only  the  more  important 
theories. 

I^aunyn  explained  the  systolic  murmur  heard  in  the  pulmo- 
nary area  in  cases  of  chlorosis  and  other  depraved  blood-states  as 
being  in  reality  due  to  mitral  regurgitation,  and  assumed  that, 
instead  of  obeying  the  law  usually  governing  its  propagation,  it  is 
conducted  along  the  left  auricular  appendix  to  the  tip,  which,  as 
we  have  seen,  lies  directly  beneath  the  chest-wall  in  front,  some- 
times overlapping  the  base  of  the  pulmonary  artery.  This  theory 
was  warmly  supported  by  Balfour,  but  appears  now  to  meet  with 
general  disapproval.  Russell  proposed  two  theories,  of  which  one 
attributed  the  murmur  to  narrowing  of  the  pulmonary  artery  by 
pressure  upon  it  of  the  dilated  left  auricle.  In  other  cases  he  be- 
lieved a  murmur  of  tricuspid  insuf-ficiency  was  transmitted  into 
the  conus  arteriosus,  which,  in  consequence  of  dilatation  of  the 
right  ventricle,  became  displaced  outward  in  the  second  left  inter- 
space. Hanford  claims  that  the  phenomenon,  which  is  either 
heard  only  or  intensified  in  the  dorsal  decubitus,  results  from  the 
pressure  upon  the  artery  of  a  flabby  and  dilated  heart.  Foxwell 
agrees  with  Russell  as  regards  pressure  in  some  cases  of  the  dilated 


28  '  DISEASES  OF  THE   HEART 

left  auricle  upon  the  artery,  but  explains  other  cases  as  due  to  a 
displacement  upward  of  the  pulmonary  artery  and  a  change  in  its 
axis  and  that  of  the  right  ventricle,  in  consequence  of  which  its 
normal  curve  is  increased  and  it  is  flattened  somewhat  against 
the  wall  of  the  chest.  Bramwell  attributes  the  murmur  to  the 
sudden  discharge  of  a  large  wave  of  blood  of  abnormal  composi- 
tion into  the  probably  dilated  artery.  Sansom  thinks  that  in  a 
condition  of  right- ventricle  weakness  toiling  to  overcome  increased 
resistance  in  the  pulmonic  system  fibrillar  tremors  can  be  initi- 
ated at  the  overstrained  portion  of  the  right  ventricle — i.  e.,  the 
conns  just  below  the  valves — and  in  this  way  the  murmur  in  ques- 
tion can  be  induced.  Gibson  holds  that  auricular  or  cardiac  dila- 
tation cannot  be  assumed  in  these  eases  because  the  murmur  oc- 
curs long  before  such  dilatation  takes  place ;  also  that  the  experi- 
ments on  which  Foxwell's  view  is  based  were  faulty ;  also  that  if 
Sansom's  theory  is  correct,  then  the  murmur  ought  to  exist  more 
often  than  it  does,  and  therefore  advocates  the  view  that  it  is  the 
murmur  of  tricuspid  insufficiency  propagated  into  the  pulmonary 
area.  Quincke,  cited  by  Balfour,  concluded,  as  a  result  of  obser- 
vations in  6  cases  of  healthy  hearts  and  arteries,  but  with  retrac- 
tion of  the  lung-borders,  that  a  systolic  basic  murmur  can  be  pro- 
duced by  pressure  by  the  heart  of  the  pulmonary  artery  against 
the  chest-wall. 

Vierordt  agrees  with  Sahli  that  in  many  cases  venous  mur- 
murs are  transmitted  from  the  great  intrathoracic  veins  to  the 
heart.  Potain  urges  the  cardio-pulmonary  origin  of  accidental 
murmurs,  maintaining  they  are  generated  by  the  impulse  of  the 
heart's  apex  against  the  lung,  an  hypothesis  that  appears  sup- 
ported by  an  observation  of  Fran(;ois-Franck's,  Avho,  during  an 
operation  upon  a  dog,  detected  a  systolic  mnrnnir  in  the  region  of 
the  apex  which  disappeared  so  soon  as  the  processus  lingualis  was 
lifted  away  from  contact  with  the  heart,  and  returned  when  this 
portion  of  pulmonary  tissue  was  allowed  to  again  rest  against  the 
surface  of  the  organ.  Such  cardio-pulmonary  origin  is  especially 
claimed  for  the  murmurs  of  ana'uiia.  Winckler,  on  the  other 
hand,  believes  he  has  discovered  the  origin  of  accidental  apex- 
bruits  in  a  defective  action  of  the  p;i])illarv  muscles  or  a  faulty 
insertion  of  the  valve-muscles,   which   |)ermits  of  regurgitation. 

Finally,  it  has  been  urged  that  these  murmurs  may  have  a 


INTRODUCTORY  29 

ha?mic  origin  in  eases  of  pernicious  and  other  grave  secondary 
anaemias,  while  opponents  of  this  view  urge  the  clinical  observation 
that  in  such  blood-states  murmurs  are  not  always  present,  and,  on 
the  other  hand,  occur  when  anaemia  does  not  exist.  Bearing  on 
this  objection  are  the  experiments  of  Thalma,  who  found  that  par- 
tial exsanguination  of  dogs  did  not  give  rise  to  accidental  mur- 
murs. A  condition  of  overfulness  of  the  vessels  caused  by  the 
injection  of  a  warm  saline  solution  into  the  femoral  vein  was 
foUov/ed  by  their  appearance. 

The  number  and  diversity  of  the  foregoing  theories  serve  but 
to  emphasize  the  sad  fact  that  in  medicine  there  are  still  many 
phenomena  which  have  to  be  accepted  as  facts,  without  a  satisfac- 
tory explanation.  In  respect  to  the  origin  of  accidental  murmurs, 
therefore,  we  can  but  place  ourselves  in  a  judicial  attitude  and 
await  further  proofs. 

Musical  Murmurs. — These  are  here  introduced  because  I  pro- 
pose to  classify  them,  not  according  to  their  acoustic  characters  or 
rhythm,  but  as  organic  and  accidental,  depending  upon  the  ana- 
tomical conditions  underlying  them.  First,  organic  musical  mur- 
murs are  those  not  infrequently  heard  in  clearly  demonstrable 
cardiac  affections,  usually  valvular.  In  their  time  they  may  be 
systolic  or  diastolic,  and  in  pitch  and  timbre  they  are  variable. 
Thus  they  are  described  as  sawing,  filing,  buzzing,  whistling,  etc. 
Their  intensity  may  be  such  that  the  patient  is  annoyed  by  the 
murmur,  and  it  is  audible  several  feet  distant,  or  it  may  require 
close  attention  for  its  detection.  Regurgitant  musical  murmurs 
are,  as  a  rule,  more  intense  than  direct  ones.  Yet  I  recall  an 
elderly  gentleman  who  presented  a  systolic  aortic  bruit  of  a  strik- 
ingly sawing  quality  so  loud  as  to  be  almost  painful  to  the  ear. 
In  the  case  of  a  negro  observed  in  my  dispensary  service  some 
years  ago  there  was  an  aortic  diastolic  murmur  which  was  audible 
a  short  distance  from  the  chest  and  had  aroused  the  wonder  of  its 
possessor.  It  was  not  constant,  and  when  present  wholly  obscured 
a  soft  diastolic  murmur  that  was  appreciable  when  the  musical 
one  was  silent.  Each  time  the  sawing  sound  was  present  it  was 
accompanied  by  a  thrill  in  the  third  left  interspace  near  the 
sternum  of  such  intensity  that  it  tickled  the  palm  of  the  palpating 
hand.  This  bruit  disappeared  some  weeks  prior  to  death,  and  at 
the  autopsy  no  cause  for  its  peculiar  quality  could  be  discovered 


30  DISEASES   OF   THE   HEART 

other  than  the  sclerotic  and  incompetent  semihniar  valves.  In 
another  man,  with  a  bruit  of  almost  identical  characters,  except- 
ing that  it  was  constant,  the  necropsy  revealed  sclerotic  aortic 
valves,  one  of  the  cusps  being  fenestrated,  and  there  being  two  thin 
fibrous  bands  stretched  between  the  edges  of  two  of  the  curtains. 
This  patient  was  a  pauper  at  the  Cook  County  Poorhouse,  and 
before  the  autopsy  could  be  made  his  body  was  confided  to  the 
tender  mercies  of  one  of  the  medical  colleges.  It  was  there  found, 
and  the  heart  secured  after  a  lapse  of  three  weeks.  The  heart 
was  injured  by  the  preserving  fluid,  pale  and  softened,  so  that 
during  the  examination  of  the  delicate  fibrous  bands  they  were 
ruptured.  Before  the  photograph  was  taken  two  threads  of  sew- 
ing cotton  were  passed  through  the  edges  of  the  valves  in  rep- 
resentation of  the  bands.  The  examination  and  preparation  of 
this  heart,  shown  in  Fig.  11,  were  made  by  Dr.  W,  A.  Evans.  In 
this  instance  the  fenestration  permitted  reflux  of  the  blood-stream 
and  the  regurgitant  wave  set  the  bands  to  vibrating,  and  thus  occa- 
sioned the  murmur  and  accompanying  thrill  over  the  body  of  the 
heart,  Engel  has  reported  a  similar  case,  in  which  a  fibrous  band 
was  stretched  across  the  aortic  orifice  to  a  pocket  of  one  of  the 
cusps. 

The  Russian,  who  under  the  name  of  Lewis  travels  from  one 
medical  school  to  another  to  exhibit  himself  to  the  students,  is  the 
proud  possessor  of  a  "  musical  heart."  In  his  case  the  singing 
bruit  is  systolic  and  of  maximum  intensity  over  the  right  ventri- 
cle, and  by  some  observers  has  been  thought  to  indicate  tricusjnd 
insufiiciency  and  to  be  generated  in  the  right  ventricle  at  the 
auriculo-ventricuhir  orifice  during  the  reflux. 

In  addition  to  fibrous  bands  or  cords,  some  of  the  conditions 
causing  a  murmur  to  have  a  musical  quality  are  said  to  be  vibra- 
tions imparted  to  the  thin,  stiflened  edge  of  a  cusp  or  fenestra- 
tion, or  to  a  delicate  atheromatous  plaque  by  the  blood-stream 
as  it  passes  over  them.  In  a  case  of  aortic  stenosis  with  a  loud 
systolic  musical  murmur  reported  by  Mayne,  two  fibrous  bands 
were  found  stretched  across  the  cavity  of  the  ventricle  just  below 
the  greatly  narrowed  orifice.  In  another  case  of  mitral  insuffi- 
ciency, which  during  life  had  exhibited  a  musical  murmur  at  the 
base  and  a  systolic  niui-mur  at  the  apex,  Potain  discovered  post 
mortem  a  cord  wjiich  passed  to  the  wall  of  the  ventricle  from  the 


INTRODUCTORY 


31 


edge  of  the  anterior  mitral  valve  just  below  the  aortic  orifice. 
Demange  reported  a  case  of  tricuspid  regurgitation  in  which  the 
musical  murmur  was  evidently  due  to  a  fibrous  band  stretched 
across  the  interior  of  the  ventricle  close  to  the  tricuspid  ring. 
Schroetter  has  suggested  that  a  musical  murmur  may  be  generated 


Fig.  11. — IxTERioR  of  Left  Vextkicle. 
Showing  fibrous  band  connecting  aortic  cusps  and  responsible  for  musical  murmur. 

by  the  vibration  of  a  tendinous  cord  swinging  free  in  the  ventricle, 
or  by  one  that,  as  a  result  of  endocarditis,  had  been  ruptured  and 
subsequently  attached  in  an  abnormal  situation.  It  is  needless 
to  remark  that  the  musical  quality  of  these  murmurs  possesses 
a  pathological  interest,  but  scarcely  a  diagnostic  significance. 
At  the  most  we  cannot  do  more  than  conjecture  their  mode  of 


32  DISEASES  OF  THE   HEART 

causation  during  life  until  the  true  condition  is  revealed  by  the 
autopsy. 

Accidental  musical  murmurs  are  rare,  and  yet  that  they  da 
occur  is  attested  by  the  following  case :  Miss  V.  was  referred  to 
me  by  Dr.  Charles  True,  of  Kankakee,  in  the  spring  of  1897,  be- 
cause of  attacks  of  intense  nervousness  and  agitation  accompanied 
by  palpitation  and  pra?cordial  pain,  for  which  no  adequate  cause 
in  the  heart  had  been  discovered.  The  patient  was  a  farmer's 
daughter,  nineteen  years  of  age,  tall  and  slender,  and  gave  no  his- 
tory of  articular  rheumatism  or  any  other  infection  that  would 
have  led  to  inflammation  of  the  cardiac  structures.  Family  his- 
tory was  also  negative.  The  girl  was  extremely  excitable  and 
unable  to  give  a  very  lucid  or  intelligent  description  of  her  symp- 
toms further  than  that  she  often  became  frightened,  at  wdiat  was 
not  at  all  clear,  apprehended  some  imaginary  danger  to  herself 
or  family,  and  had  rapid  beating  of  the  heart.  During  my  ex- 
amination she  was  much  agitated,  and  the  heart  action  was  greatly 
accelerated,  about  120,  but  perfectly  regular.  The  area  of  cardiac 
dulness,  both  superficial  and  deep,  was  not  increased,  but  there 
was  a  blowing  systolic  murmur  at  the  apex,  the  heart-sounds  being 
sharp  and  ringing.  She  was  moderately  anaemic,  and  there  was  a 
slight  enteroptosis.  Aside  from  a  not  very  troublesome  fermenta- 
tive indigestion  and  constipation,  her  functions  appeared  to  be 
normal  and  the  urine  was  negative.  The  case  was  considered  one 
of  cardiac  neurosis,  the  murmur  accidental,  and  treatment  con- 
sisted of  haematics,  laxatives,  and  remedies  designed  to  lessen  the 
indigestion.  The  patient  was  seen  by  me  at  rather  infrequent 
intervals,  and  each  time  appeared  to  be  somewhat  improving.  Re- 
peated examinations  of  the  heart  failed  to  elicit  anything  more 
than  at  her  first  visit,  and  the  murmur  subsequently  disappeared. 
On  one  occasion,  however,  she  seemed  more  than  ordinarily  per- 
turbed, and  her  pulse  was  more  rapid  than  I  had  ever  seen  it. 
During  my  examination  of  the  heart,  which  was  always  made  as  a 
matter  of  routine,  I  was  astonished  to  hear  over  the  body  of  the 
right  ventricle  a  distinct,  short,  exquisitely  twanging  murmur  of 
very  high  ])itch  and  pleasing  quality.  It  seemed,  as  well  as  the 
tachycardia  would  allow  me  to  judge,  of  a  systolic  rhythm.  The 
action  of  the  heart  at  the  time  was  extremely  rapid  and  violent. 
This  interesting,  and  to  me  exceptional,  phenomenon  lasted  for 


INTRODUCTORY 


33 


several  minutes,  indeed  so  long  as  the  rapidity  of  cardiac  action 
endured.  When  at  length  her  pulse  grew  more  quiet  the  musical 
murmur  became  inaudible  and  did  not  reappear.  This  patient 
was  seen  by  me  in  Septe^nber,  1900,  after  a  lapse  of  more  than  a 
year  from  her  last  visit,  and  although  I  diligently  sought  for  the 
twanging  sound  and  any  signs  of  cardiac  disease,  I  failed  to  detect 
any  abnormality.  The  patient  reported  herself  as  in  much  better 
health  and  less  excitable,  being  but  rarely  annoyed  by  her  former 
symptoms,  and  indeed  appeared  not  the  least  disturbed  by  the 
examination. 


Fig.  12. — Heart  of  a  Buffalo  Calf. 
Showing  aberrant  chordfe  tendinee  in  left  ventricle. 

The  only  explanation  that  has  seemed  to  account  for  this  re- 
markable phenomenon  is  that  the  musical  murmur  was  due  to  the 
vibration  of  one  of  the  so-called  aberrant  cords  (Fig.  12)  or  mod- 


34  DISEASES   OF   THE   HEART 

ernlor  hands,  desoribcJ  l)v  H.  F.  Lewis.  These  cords  are  thin 
librons  bands  ruiming  along  the  inner  aspect  of  the  wall,  or 
stretched  across  the  upper  part  of  the  cavity,  or  from  a  })apillary 
muscle  to  the  sa^ptum.  They  have  nothing  to  do  with  the  chordne 
tendina?,  and  unless  care  is  taken,  may  be  cut  in  the  opening  of 
the  ventricle  and  thus  escape  detection.  Although  most  frequent 
in  the  left,  they  have  been  found  in  the  right  ventricle,  and  there 
are  instances  of  such  a  band  passing  from  the  valve  of  the  fora- 
men ovale  into  the  cavity  of  the  left  ventricle  and  attached  to  a 
leaf  of  the  mitral  valve.  It  is  supposed  that  the  function  of  these 
moderator  bands  is  to  strengthen  the  cardiac  walls  in  times  of 
overstrain.*  In  the  case  narrated  it  is  assumable  that  owing  to 
the  tachycardia  the  cardiac  chambers  became  overfilled  and  an 
aberrant  cord  was  thus  put  on  the  stretcli.  In  this  state  of  ten- 
sion it  was  set  to  vibrating  by  the  energetic  and  rapid  cardiac  con- 
tractions, thus  generating  the  twanging  murmur,  like  that  of  a 
violin-string  twitched  by  the  finger  of  the  musician.  Lewis  says 
it  is  these  al)errant  cords  which  are  responsible  for  the  systolic, 
sometimes  diastolic,  musical  murmur  heard  before  death.  Several 
of  the  musical  murmurs  observed  in  connection  with  valvular  de- 
fVets  have  apparently  been  due  to  alierrant  fibrous  l)ands,  so  situ- 
ated as  to  linve  been  thrown  into  vibration  by  the  ])lood-stream. 
The  Diflferential  Diagnosis  of  Accidental  Heart  Murmurs. — Un- 
<ler  some  circumstances  it  uuiy  be  difficult  to  differentiate  these 
from  organic  murmurs.  The  patient's  ananmesis  is  to  be  care- 
fully considered,  since,  if  inquiry  fails  to  elicit  a  history  of  ar- 
ticular rheumatism  or  any  infectious  disease  likely  to  liave  set  up 
an  endocarditis,  it  furnishes  some  evidence  in  favour  of  the  non- 
organic nature  of  tlie  murmur.  This  is  strengthened  if  the  ]xi- 
tient  is  neurotic,  ana'mic,  or  chlorotic,  if  there  are  digestive  or 
pelvic  disorders  likely  to  produce  disturbance  through  the  sym- 
pathetic nervous  system,  if  l)ecause  of  n(M"vousness  the  heart's  ac- 
tion is  excited  or  if  there  is  a  history  of  cardiac  overstrain.  If  the 
individual  is  given  to  vicious  habits,  as  sexual  excesses  of  one  kind 


*  The  investigations  of  Aschoff  and  Tawara  into  the  course  taken  by  the  fibres 
♦•ondiK'ting  impulses  from  aurielos  to  ventricles  and  composing  the  so-called  bun- 
dle of  His,  have  proved  that  these  abnormal  bands  stretching  across  the  interior  of 
a  ventricle  or  from  the  sei)tum  to  the  posterior  papillary  nmscle  are  in  reality 
branches  of  the  conducting  system  whicli  have  taken  a  wrong  direction. 


INTRODUCTORY  35 

or  another,  particularly  masturbation,  or  indulges  too  freely  in 
tobacco,  tea,  or  coffee,  the  presumption  is  strengthened  that  the 
murmur  is  accidental.  Of  course,  these  and  numerous  other  fac- 
tors that  are  said  to  afford  ■prima  facie  evidence  of  the  malady 
being  not  organic  may  exist  in  a  given  case  with  an  endocardial 
murmur  of  ^^alvular  disease.  There  must,  therefore,  be  made  a 
careful  examination  of  the  heart  and  other  viscera. 

It  may  be  stated  as  a  general  proposition  that  accidental  mur- 
murs are  not  accompanied  by  secondary  changes  in  the  size  of  the 
heart  or  by  circulatory  disturbances,  such  as  generally  attend  and 
depend  upon  valvular  affections.  The  discovery  of  hypertrophy 
or  dilatation  of  the  heart  makes  strongly  for  the  organic  and 
against  the  accidental  origin  of  a  murmur.  Smallness,  feebleness, 
and  intermittence  of  the  pulse,  cyanosis,  dyspnoea  of  effort,  hepatic 
and  other  visceral  engorgement,  etc.,  are  not  usual  accompani- 
ments of  accidental  murmurs.  Such  signs  of  serious  embarrass- 
ment of  the  circulation  failing,  information  may  be  sought  for  in 
the  rhythm  and  other  characters  of  the  murmur  itself.  Accidental 
bruits  of  cardiac  origin  are  rarely  if  ever  diastolic,  whereas  or- 
ganic ones  may  occur  during  any  or  all  phases  of  the  cardiac  cycle. 
Leube  has  never  heard  such  a  diastolic  accidental  murmur,  and 
doubts  its  occurrence.  Although  these  murmurs  may  exist  in  any 
portion  of  the  pritecordia,  they  are  most  frequent  over  the  base,  in  or 
near  the  pulmonary  area,  and  next  in  frequency  at  the  apex  in  the 
mitral  region.  In  transmission  they  are  usually  rather  limited,  and 
such  an  apex-bruit  is  not  propagated  to  the  angle  of  the  left  scapula. 

Organic  murmurs,  on  the  contrary,  occur  with  frequency  in 
all  areas,  and  often  have  a  wide  extent  of  audibility  besides  being 
propagated  in  definite  directions  and  to  considerable  distances.  In 
the  matter  of  intensity,  murmurs  of  both  organic  and  accidental 
origin  are  variable.  Leube  is  of  the  opinion  that,  as  a  rule,  the 
latter  are  the  less  loud  of  the  two,  but  the  reverse  occasionally 
obtains.  The  murmur  of  chlorosis  and  anaemia,  so  often  spoken 
of  as  hsemic,  which  is  heard  chiefly  in  the  pulmonic  area,  is  gen- 
erally intensified  in  the  dorsal  decubitus,  while  Drummond  states 
correctly,  I  believe,  that  the  ''  neurotypic  "  (cardio-muscular) 
becomes  less  pronounced  after  rest  in  the  recumbent  posture  has 
slowed  the  heart.  This  latter  type  is  most  intense  during  ex- 
citement and  in  the  standing  position.     The  same  is  true  of  the 


36  DISEASES  OF  THE   HEART 

cardio-piilmonarj  murmur.  These  last  two  diminish  or  disap- 
pear in  the  lateral  decubitus,  particularly  when  the  patient  lies 
on  his  right  side.  Organic  bruits  never  wholly  cease  in  the  re- 
cumbent or  lateral  position.  I\espiratory  movements  also  affect 
the  intensity  of  accidental,  but  not  the  organic  murmurs.  The 
basic  chlorotic  bruit  is  loudest  at  the  end  of  forced  expiration,  and 
at  the  close  of  deep  inspiration  may  cease  entirely.  A  neuro- 
typic  (eardio-muscular)  murmur  is  also  intensified  at  the  end  of 
forced  expiration,  and  less  or  absent  at  the  close  of  a  deep  inspira- 
tory effort.  The  cardio-pulmonary  or  cardio-respiratory  murmur^ 
on  the  other  hand,  is  influenced  conversely,  being  loudest  at  end 
of  forced  inspiraiion  and  weakest  at  end  of  deep  expiration,  or 
ceases  when  the  patient  holds  his  breath. 

The  pitch  of  accidental  murmurs  is  usually  higher  than  that 
of  the  organic,  3'et  is  rarely  musical,  and  may  occasionally  be 
lower.  In  quality  the  former  is  apt  to  be  softer,  yet  may  be  harsh, 
even  grating,  and  the  apex-bruit  in  neurotic  individuals  is  not  in- 
frequently vibrant  or  '^  whizzing"  (Drummond),  and  may  be  ac- 
companied by  a  systolic  thrill  in  the  upright  position  or  when  the 
murmur  is  the  loudest  during  excitement.  Finally,  the  pulmonic 
second  sound  is  not  so  accentuated,  as  a  rule,  in  accidental  mur- 
murs as  in  mitral  systolic  bruits  of  organic  origin.  The  reason  is 
obvious;  in  the  former  there  is  not  the  same  likelihood  of  sec- 
ondary pulmonary  hyperai'mia.  This  lessened  intensity  of  the 
pulmonary  second  sound  goes  hand  in  hand  with  the  absence  of 
appreciable  enlargement  of  the  right  ventricle. 

In  a  considerable  proportion  of  cases  a  definite  opinion  cannot 
be  expressed  at  the  first  sitting,  and  must  be  reserved  until  the  pa- 
tient has  become  accustomed  to  an  examination  or  has  grown  less 
nervous,  or  until  after  the  results  of  treatment  have  been  observed. 

Exocardial  Murmurs. — The  pericardial  friction-sounds  that 
come  under  this  head  will  be  found  fully  considered  in  the  appro- 
priate chapter.  Pleuro-])('ricardial  murmurs  may  result  from  the 
friction  of  the  heart  on  the  roughened  surface  of  the  pleura,  where 
it  comes  in  contact  witli  tlic  fornici-.  Their  differentiation  from 
pericardial  or  endocardial  murmurs,  which  they  may  at  times 
simulate  because  of  the  rhythm,  is  usually  accomplished  by  having 
the  patient  hold  his  breath,  when  the  friction-sound  disappears. 
A  deep  inspiration  often  increases  its  intensity. 


SECTION  I 
DISEASES   OF  THE   PEEICAEDIUM 


CHAPTER    I 

ACUTE   PERICARDITIS 

Morbid  Anatomy. — The  pericardium  is  a  closed  sac  lined 
with  serous  membrane  which  surrounds  the  heart,  a  visceral  layer 
of  the  serosa  (the  epicardium)  being  reflected  over  the  surface 
of  that  organ,  and  for  a  short  distance  along  the  roots  of  the  great 
blood-vessels.  The  parietal  layer  of  endothelium  is  re-enforced  by 
a  strong  fibrous  lamina,  extending  from  the  diaphragm  below,  to 
be  continuous  with  the  fibrous  sheaths  of  the  great  vessels  above. 
The  pericardial  sac  usually  contains  after  death  a  few  drachms 
(10  to  15  cubic  centimetres)  of  a  clear  straw-coloured  fluid. 

An  inflammatory  process  of  the  pericardium  may  involve  only 
the  serosa,  or  may  penetrate  into  the  myocardium  or  into  the 
fibrous  tissue  of  the  parietal  layer.  It  may  involve  the  entire  sur- 
face or  it  may  confine  itself  to  limited  areas,  single  or  multiple, 
thus  giving  rise  to  the  circumscribed  form  of  the  disease.  The 
morbid  anatomical  condition  is  the  same  in  the  two  forms  except 
in  the  extent  of  involvement,  and  the  same  description  applies  to 
both. 

The  first  evidence  of  inflammation  is  the  injection  of  the  blood- 
vessels lying  beneath  the  transparent  serous  membrane,  the  process 
usually  beginning  in  the  parts  of  the  sac  surrounding  the  great 
vessels.  This  is  associated  with  considerable  desquamation  of  the 
endothelium,  which  gives  an  appearance  that  is  described  as  of 
having  been  breathed  upon.  As  the  endothelial  cells  are  those 
which  lubricate  the  surfaces,  this  desquamation  occasions  friction 
between  the  two  layers  of  the  sac,  giving  rise  to  the  sounds  that 
are  heard  during  life.     This  is  the  simplest  form  of  pericarditis, 

37 


38  DISEASES   OF   THE    HEART 

and  the  disease  may  proceed  no  farther.  Usually,  however,  exuda- 
tion occurs,  and  the  formation  of  the  exudate  is  in  many  cases  the 
prominent  feature  of  the  disease.  The  character  of  the  exudate 
varies  extremely.  It  may  be  fibrinous,  serous,  purulent,  or  hsem- 
orrhagie,  sero-fibrinous,  or  hbrino-purulent.  In  fact,  almost  any 
combination  may  occur. 

In  the  fihrinous,  dry,  or  plastic  form  the  exudate  appears  at 
first  as  a  thin  smooth  pellicle,  of  a  grayish-white  or  yellowish- 
white  colour,  easily  detached  from  the  injected  surface  beneath. 
Later  the  exudate  becomes  thicker,  and  is  of  a  pasty  consistence, 
and  not  so  easily  detached  from  the  underlying  surface.  The 
incessant  motion  of  the  heart  causes  the  plastic  exudate  to  assume 
forms  that  have  been  variously  described  by  different  authors.  A 
common  condition  is  one  resembling  the  appearance  produced  by 
tearing  apart  two  pieces  of  tliickly  buttered  bread.  At  other 
times  fine  threads  of  fibrin  attaclied  all  over  the  surface  of  the 
pericardium  give  to  the  heart  the  shaggy  or  hairy  appearance  that 
has  received  the  names  of  cor  hirsatum,  cor  villosinn,  and  cor 
tomentosum  (Fig.  13).  In  still  other  instances  the  fibrin  is  ar- 
ranged in  coarser  masses  of  the  characteristic  grayish-yellow  col- 
our. Such  an  exudate,  being  in  contact  with  both  layers  of  the 
pericardial  sac,  forms  between  them  adhesions  of  the  kind  de- 
scribed as  recent  oi-  fibrinous,  in  contradistinction  to  the  old  or 
fibrous  adhesions  found  in  the  chronic  form.  The  appearances 
described  are  to  some  extent  the  result  of  the  tearing  apart  of  the 
two  layers  of  tlie  sac,  thus  loosely  boimd  together.  The  processes 
leading  to  the  repair  of  this  lesion  are  those  eventuating  in 
chronic  pericarditis,  and  are  considered  in  that  connection.  Ac- 
cording to  Osier,  plastic  pericarditis  is  frequently  tuberculous,  but 
the  tubercles  are  very  easily  overlooked  in  the  presence  of  the 
fibrinous  exudate. 

When  the  exudate  into  the  cavity  is  of  a  fluid  nature  the  con- 
dition is  known  as  pericarditis  with  effusion.  The  effusion  may 
be  serous,  purulent,  or  liipmorrhagic  in  character,  but  the  most 
commonly  occurring  condition  is  that  in  which  the  effusion  shows 
mixed  or  intermediate  characters.  In  the  serous  form  there  is  an 
effusion  of  serum  from  the  inflamed  surface,  wliidi  may  be  per- 
fectly clear,  but  more  commonly  contains  fibrin  in  the  form  of 
shreds,  flakes,  or  larger  masses,  which  may  float  in  the  fluid,  or 


Fig.  13. — Cor  Villosum  of  Acute  Plastic  Pericarditis. 
Photograph  of  specimen  in  Museum  of  Cook  County  Hospital. 

39 


40  DISEASES  OF  THE  HEART 

may  be  deposited  on  the  walls  of  the  sac  as  a  creamy  layer.  This 
is  the  form  of  the  disease  known  as  sero-fihrinous  pericarditis,  and 
is  the  one  most  commonly  met  with.  It  usually  begins  as  a  dry 
pericarditis,  the  effusion  developing  later,  and  indeed  in  the  dry 
form  there  is  aways  some  transudation  of  fluid,  although  its 
amount  is  insignificant  compared  to  that  of  the  fibrin.  The  fluid 
is  often  slightly  turbid  from  the  presence  of  leucocytes,  but  in 
insufficient  number  to  entitle  the  eftusion  to  be  called  purulent,  or 
a  small  proportion  of  blood  may  give  to  the  fluid  a  reddish  or 
brownish  tinge.  The  amount  of  fluid  varies  from  a  few  ounces  to 
several  pints. 

In  the  purulent  form  the  effusion  is  rich  in  cells,  and  of  a 
thick,  creamy  consistence,  but  all  degrees  of  variation  exist  be- 
tw^een  this  form  and  that  presenting  a  serous  exudate  with  slight 
turbidity  from  the  presence  of  j)us-cells,  so  that  a  sharp  line  can- 
not always  be  drawn  between  the  two  conditions.  When  the  effu- 
sion is  truly  purulent  the  condition  is  practically  an  abscess,  and 
the  pus  may  burrow  and  rupture  externally,  as,  for  instance,  in 
the  first  right  interspace,  or  in  the  neck  above  the  clavicle.  The 
condition  is  a  serious  one,  and  shows  but  little  tendency  to  resorp- 
tion, and  yet  the  pus  may  become  inspissated  and  calcified. 

In  the  hcemorrhagic  form  the  effusion  contains  a  large  propor- 
tion of  blood,  or  even,  as  in  scurvy,  may  seem  to  be  composed  of 
pure  blood.  In  cases  of  long  standing  the  decomposition  of  the 
hiemoglobin  gives  the  fluid  a  brownish  rather  than  a  red  colour. 
Aside  from  the  scorl)utic  form,  ha-morrhagic  j)ericarditis  occurs 
most  often  associated  with  tuberculosis  of  the  pericardium  and 
with  malignant  disease.  The  effusion  is  usually  very  large,  and 
may  take  place  so  suddenly  as  to  produce  the  symptoms  of  acute 
secondary  ana-mia. 

Various  bacteria  have  been  found  in  the  exudates  of  acute 
pericarditis,  including  the  various  pyogenic  organisms,  the  diplo- 
coccus  pneumonia',  and  the  l)acillus  tuberculosis,  but  it  is  not 
always  possible  to  demonstrate  bacteria.  The  presence  of  organ- 
isms causing  putrefaction  may  give  to  the  effusion  a  foul  odour. 
The  Bacillus  aerogenes  capsulatus  may  produce  gas  in  the  })eri- 
cardium.  This  production  of  gas  is  probably  a  post-mortem 
change  (Osier),  but  according  to  Cojdin  (1S09)  occurs  during 
life. 


ACUTE  PERICARDITIS  41 

Secondary  changes  are  found  mainly  in  the  myocardium, 
which  nuiy  show  inflammatory  infiltration,  or  a  fatty  or  albumi- 
nous degeneration  of  its  muscle-fibres,  leading,  after  the  acute 
stage  has  passed,  to  an  insterstitial  myocarditis.  There  may  be 
evidence  of  recent  disease  of  the  endocardium,  usually  due  to  the 
same  morbific  agency  as  the  pericarditis.  Associated  disease  of 
the  lungs  or  pleurae  usually  bears  an  etiologic  relation  to  the  dis- 
ease of  the  pericardium.  If  there  has  been  high  fever,  the  vari- 
ous parenchymatous  organs  show  cloudy  swelling. 

Etiology. — If  one  compare  the  statements  of  older  authors 
with  those  of  modern  writers  concerning  the  causation  of  acute  peri- 
carditis, the  chief  dift'erence  that  will  impress  him  will  be  found 
in  the  change  of  views  regarding  the  frequency  of  the  primary  as 
opposed  to  the  secondary  form  of  this  affection.  The  term  pri- 
mary was  made  to  include  those  cases  regarded  as  idiopathic  or  of 
spontaneous  origin.  A  better  knowledge  of  pathology  and  etiol- 
ogy, founded  on  the  results  of  bacteriological  investigation,  has 
taught  us  the  fallacy  of  a  belief  in  spontaneous  development  of 
disease.  Authors  now  restrict  primary  inflammation  of  the  peri- 
cardium to  those  cases  originating  in  trauma,  and  include  among 
the  secondary  all  other  cases  once  considered  primary  or  idio- 
pathic. This  is  undoubtedly  due  in  part  to  a  more  accurate  knowl- 
edge, and  therefore  more  frequent  recognition,  of  the  rheumatic 
nature  of  many  disorders  whose  pathology  was  formerly  but  indis- 
tinctly understood — as,  for  instance,  certain  rheumatic  nodules 
occurring  in  childhood.  The  chief  reason,  however,  is  to  be  found 
in  the  remarkable  additions  made  to  our  knowledge  during  the 
past  twenty  years  or  so  regarding  the  pathology  and  bacteriology 
of  disease,  above  referred  to.  At  present  the  physician  would  be 
far  behind  the  times  who  failed  to  recognise  inflammation  of  the 
pericardium  as  a  local  manifestation  of  a  general  constitutional 
disease  or  as  a  secondary  infection  in  the  course  of  some  disease 
having  pathogenic  organisms  as  an  etiological  factor.  Tor  in- 
stance, the  primary  pericarditis  that  was  formerly  thought  to  fol- 
low exposure  or  chill  was  probably  due  to  a  rheumatic  attack,  the 
true  nature  of  which  escaped  recognition. 

Furthermore,  some  of  the  cases  of  pericarditis,  formerly  re- 
garded as  idiopathic,  were  observed  in  individuals  whose  general 
resistance  had  been  greatly  reduced  by  privation  or  chronic  alco- 


42 


DISEASES   OF  THE   HEART 


holism.  In  such  the  pericardial  inflainination  was.  properly  speak- 
inflf,  due  to  infection.  The  sero-fibrinous  ix'ricavditis  arisins;  in 
the  course  of  articular  rheumatism  is  a  local  expression  of  the 
rheumatism,  and  the  suppurative  pericarditis  sometimes  seen  in 
puerperal  septicnemia  is  due  to  the  primary  infection.  Roberts 
goes  so  far  as  to  say:  "In  my  own  experience  I  have  never  met 
with  an  instance  of  acute  pericarditis  which,  when  carefully  inves- 
tigated, could  not  be  included  as  a  secondary  event  in  one  or  other 
of  the  etiological  groups  now  to  be  discussed."  Among  these,  he 
includes  pericarditis  from  extension  or  irritation,  from  trauma  and 
perforation,  from  cardiac  and  aortic  disease,  and  those  associated 
with  new  growths,  general  miscellaneous  diseases,  and  blood- 
states. 

In  his  investigations  regarding  "  terminal  infections "  in 
chronic  disease,  Flexner  has  made  some  highly  interesting  and 
important  observations  with  reference  to  the  etiology  and  bac- 
teriology of  acute  pericarditis.  I  cannot  do  better  than  to  repro- 
duce one  of  his  tables,  which  gives  the  frequency  with  which  cer- 
tain bacteria  were  found  and  their  point  of  entrance : 


Bacteria. 

Frequency. 

Infection  Atrium. 

Micrococcus  laiiccolatus 

11 
4 
1 
1 

1 
1 

1 

1       • 

Pneumonia,  8  times. 

Streptococcus 

Stiipliylococcus  aureus             

Bronciiitis,  2  times. 
KrysijK'las,  1  time. 
Lcfi;  ulcer,  1  time. 

Hiicillus  pyocyaueus              .  .                    

Micrococcus  lanceolatus  and  Bacillus  coli.  . 
Bacillus  influenziB 

Peritonuium,  1  time. 
Tonsils,  1  time. 

Streptococcus,  Staphylococcus  aureus,  and  I 

I'acillus  coli ) 

Stujilivlococcus  and  Bacillus  coli 

Cancer,  stomach,  1  time. 
Sloufi^hiiio;  myoma,  1  time. 

Unidentified  bacilli 

Doubtful. 

Tubercle  bacilli  should  be  added  to  this  list.  From  the  fore- 
going it  is  plain  that  acute  pericarditis  may  be  a  secondary  infec- 
tion following  a  great  variety  of  local  infectious  processes,  or  it 
may  arise  in  the  course  of  an  infectious  disease,  and  be  due  to  the 
pathogenic  organism  of  that  disease. 

Rheumatism. — All  observers  agree  in  placing  articular  rheu- 
matism first  in  tlie  list  of  those  affections  which  give  rise  to  acute 
pericarditis.  The  certainty  of  this  connection  was  established  by 
Pitcairn  in  1788,  although  liis  views  were  first  widely  published 
in  1795.     Writers  have  been  in  accord  concerning;  their  causative 


ACUTE  PERICARDITIS  43 

connection,  yet  there  has  been  great  diversity  of  opinion  regard- 
ing the  frequency  with  which  pericarditis  occurs  in  the  course  of 
rheumatism ;  whether  it  occurs  most  frequently  in  the  first  or  sub- 
sequent attacks;  whether  it  is  most  likely  to  be  associated  with 
inflammation  of  one  or  several  joints,  or  any  particular  joint; 
whether  with  chronic  as  well  as  acute  articular  inflammation ;  and 
whether  or  not  it  precedes  or  follows  or  develops  coincidently 
with  the  joint  affection.  Concerning  the  first  of  these  questions, 
it  is  generally  held  that  pericarditis  occurs  less  frequently  than 
endocarditis,  yet  there  is  a  wide  divergence  in  the  figures  given 
by  authors  regarding  its  numerical  relation  to  attacks  of  rheuma- 
tism. Chambers  gave  it  as  occurring  in  13  per  cent,  Ormerod  in 
71.7  per  cent,  Bamberger  in  30  per  cent,  while  Bauer,  although 
believing  exact  figures  cannot  be  stated,  considered  from  16  to  20 
per  cent  not  far  from  the  truth.  Of  Poynton's  150  fatal  cases  of 
rheumatic  heart  disease  in  children,  he  found  evidence  of  pericar- 
ditis in  113  cases  (75  per  cent).  Personally,  I  regard  such  statis- 
tics as  of  but  small  value,  and  consider  it  sufficient  to  state  in  gen- 
eral terms  that  rheumatism  is  so  frequently  complicated  by  acute 
pericarditis  that  in  every  case  of  the  former  affection  the  medical 
attendant  should  keep  a  sharp  lookout  for  the  development  of 
pericardial  inflammation.  Most  authors  agree,  I  think,  in  the 
opinion  that  pericarditis  is  more  apt  to  occur  in  the  first  and 
endocarditis  in  the  subsequent  attacks  of  articular  rheumatism. 
Bauer  asserts  that  it  bears  no  definite  i^elation  to  the  number  of 
joints  affected  nor  to  the  involveinent  of  any  particular  joint.  It 
certainly  does  not  occur  more  frequently  in  rheumatism  of  the 
upper  than  of  the  lower  extremities.  The  last-named  author  states 
emphatically,  also,  that  it  does  not  occur  in  the  course  of  chronic 
rheumatism,  nor  when  but  a  single  joint  is  affected.  The  devel- 
opment of  acute  pericarditis  is  by  others  thought  more  likely  in 
the  severe  forms  of  the  rheumatic  affection,  and  therefore  when 
a  number  of  joints  become  attacked. 

Although  such  a  relationship  between  acute  pericarditis  and 
severe  rheumatisirx  Avas  noticed  by  Sibson,  it  was  not  constant. 
In  children  rheumatic  manifestations  are  often  mild,  and  yet  the 
little  ones  do  not  escape  pericardial  inflammation.  In  one  case 
coming  under  my  notice  the  pericarditis  followed  no  other  evi- 
dences of  rheumatism  than  vague  pains  in  the  knees,  with  ery- 


44  DISEASES  OF   THE  HEART 

tlienia  accoinpanicd  by  mild  fever,  these  symptoms  having  been 
preceded  by  follicular  tonsillitis. 

There  are  no  constant  time  relations,  moreover,  between  an 
attack  of  rheumatism  and  inflammation  of  the  pericardium.  The 
latter  may  even  precede  the  former,  although  it  most  commonly 
develops  during  or  after  the  rheumatism.  It  generally  makes  its 
appearance  from  the  fourth  to  the  sixth  day  of  the  rheumatic  dis- 
order, sometimes  not  before  the  tenth  or  lifteenth  day,  and  has 
even  been  known  by  Sibson  to  be  postponed  as  long  as  the  sixty- 
third  day.  Rheumatic  pericarditis  may  exceptionally  attack  in- 
dividuals of  all  ages,  but  is  undeniably  most  frequent  in  young 
adults  who  have  been  rendered  susceptible  to  it  by  hard  work  or 
exposure.  In  England  it  appears  to  be  particularly  prevalent 
among  young  servant-girls  below  the  age  of  twenty-one  (Sibson), 
and  among  persons  of  both  sexes  thus  afflicted  at  a  later  age,  the 
majority  were  found  by  the  same  author  t«  follow  more  or  less 
laborious  outdoor  occupations. 

Its  ])revalence  among  children  is  shown  by  statistics  gathered 
from  children's  hospitals  by  Sturgcs  and  Poynton.  Yet  Roberts 
states  that,  according  to  his  experience,  pericarditis  is  very  much 
less  frequent  in  children  of  the  better  classes,  a  fact  which,  he  be- 
lieves, shows  the  predisposing  influence  of  hardship,  not  alone  in 
the  production  of  rheumatism,  but  also  in  the  development  of  peri- 
carditis. 

Satisfactory  evidence  of  the  infectious  nature  of  the  rheumatic 
poison  has  not  yet  been  adduced,  although  many  observers  have 
expressed  the  belief  that  the  pathogenic  organism  will  yet  be  dis- 
covered. If  such  an  organism  should  one  day  be  identified,  then 
pericarditis  would  no  longer  be  considered  a  complication,  but  a 
natui-al  thougli  not  a  necessary  part  of  the  pathological  process  of 
iiilhiiiiiiiatoi'v  rhcuuuitisui. 

Nephritis. — The  importance  attached  to  renal  disease  in  tlie 
production  of  acute  pericarditis  is  scarcely  appreciated,  I  think, 
by  the  majority  of  physicians.  A  few  writers  of  wide  clinical 
experience  place  nephritis  as  only  second  in  this  regard  to  inflam- 
matory rheuinatisui.  It  should,  however,  yiehl  ])lace  to  acute 
])neunionia  in  this  regard.  The  |)ericardial  inllauiiuation  is  not 
limited  to  acute  ncjjliritis,  as  might  be  su])]>osed,  from  the  fact  that 
the  latter  is  so  frequently  observed  in  the  course  of  acute  infec- 


ACUT^E   PERICARDITIS  45 

tious  diseases,  but  may  apj^ear  during  the  progress  of  any  one  of 
the  chronic  forms  of  kidney  disease.  Indeed,  it  is  said  to  be  a 
specially  frequent  complication  of  the  small  red  kidney.  Ursemia 
seems  to  particularly  predispose  to  acute  pericarditis,  while  the 
supervention  of  the  latter  contributes  largely  to  the  fatal  termina- 
tion of  the  primary  affection.  Most  authors  content  themselves 
with  a  statement  of  the  fact  and  make  no  attempt  to  explain  the 
well-known  etiological  connection  between  acute  or  chronic  in- 
flammation of  the  kidney  and  inflammation  of  the  pericardium. 
Two  explanations  may  be  given,  however.  By  some  the  blood  of 
nephritic  patients  is  thought  to  contain  some  noxious  substance, 
possibly  of  chemical  nature,  possibly  of  catabolic  origin,  which 
results  from  renal  disease,  and  which  in  consequence  of  renal 
inadequacy  is  not  excreted.*  This  noxa  is  an  irritant,  and  gain- 
ing access  to  the  pericardial  cavity,  there  sets  up  an  irritative  in- 
flammation. Givadinovitch  expresses  the  opinion  that  acute  peri- 
carditis in  Bright's  disease  is  of  true  toxic  nature.  It  is  mostly 
fibrinous,  but  may  be  haemorrhagic  and  very  rarely  sero-fibrin- 
ous,  and  always  occurs  in  an  advanced  stage  of  the  renal  dis- 
ease. According  to  the  other  less  conservative  explanation,  peri- 
carditis is  a  true  secondary  infection,  caused  by  the  conveyance 
to  the  pericardium  of  germs  circulating  in  the  blood,  and  re- 
sponsible for  the  acute  or  chronic  pericarditis.  In  cases  of  the 
small  red  kidney,  it  is  assumed  that  invasion  of  the  pericardium 
by  bacteria  takes  place  either  because  the  renal  disease  has  im- 
paired the  germicidal  action  of  the  blood,  or  because  it  interferes 
with  the  proper  elimination  of  the  micro-organisms. 

Apropos  of  the  statement  that  infection  frequently  occurs  in 
Bright's  disease,  Flexner's  observations  may  again  be  quoted.  Of 
32  cases  of  chronic  nephritis  occurring  alone,  in  which  there  was 
general  infection,   micro-organisms  were  positively  identified  in 

*  Chatin  has  reported  four  cases  of  pericarditis  in  patients  suffering  from 
nephritis.  In  three  cases  with  effusion  bacteriologic  examination  showed  the 
fluid  to  be  sterile.  In  these  three  cases  the  serum  was  hypertoxic.  The  toxic 
elements  supposed  to  be  responsible  for  the  inflammation  of  the  pericardium  have 
been  found  neither  in  the  circulating  blood  nor  in  the  effusion ;  and  the  existence 
of  aseptic  and  amicrobie  pericarditis  in  certain  cases  of  Bright's  disease  is  well 
established.  The  pericarditis  of  nephritis  may  sometimes  develop  as  a  complica- 
tion of  an  ordinary  infection,  and  is  usually  aseptic  or  sterile. — Revue  de  medecine, 
July  10,  1900. 


46  DISEASES  OF  THE   HEART 

29.  It  is  worthy  of  note,  however,  that  in  none  of  these  cases 
was  pericarditis  present.  On  the  dflier  hand,  pericarditis  was 
found  23  times  in  cases  of  chronic  nephritis  in  which  there  was 
local  infection,  whether  the  nephritis  existed  alone  or  in  combina- 
tion with  some  other  chronic  disease,  as  of  the  heart  or  liver.  It 
would  seem,  therefore,  that  although  a  general  infection  may  occur 
in  the  course  of  chronic  nephritis,  pericarditis  does  not  take  place 
unless  there  be  some  other  local  infection.  In  the  majority  of 
cases  of  pericarditis  in  the  course  of  chronic  nephritis  there  was 
pneumonia,  either  croupous  or  lobular.  It  may  be  queried,  there- 
fore, whether  the  pericardial  inflammation  is  not  secondary  to  the 
local  infection  rather  than  to  the  nephritis  itself. 

Acule  Pneumonia. — This  infection  should  certainly  be  given 
a  place  only  subordinate  to  articular  rheumatism  in  the  etiology 
of  acute  pericarditis.  The  frequency  of  this  association  has  been 
recognised  by  authors,  but  has  been  brought  out  with  special  clear- 
ness by  Preble,  who  found  pericarditis  in  92.4  per  cent  of  79  cases 
of  fatal  pneumonia  collected  from  the  post-mortem  records  of 
Cook  C^ounty  Hospital.  Preble  came  to  the  conclusion  that  the 
danger  of  pericarditis  bears  a  direct  relation  to  the  extent  of  lung 
involvement,  and  is  also  relatively  more  frequent  in  left-sided 
than  right-sided  pneumonias.  The  inflammation  of  the  pericar- 
dium may  result  from  direct  extension  through  the  lymphatics  or 
may  occur  independently,  and  is  due  to  the  pneumococcus,  which 
has  been  frequently  identified  in  the  exudate. 

Scarlatina. — This  is  sometimes  complicated  by  the  occurrence 
of  acute  pericarditis,  and  in  some  cases  this  has  taken  place  dur- 
ing the  stage  of  desquamation.  As  the  scarlatinal  organism  has 
not  been  identified  in  the  pericardial  effusions,  this  latter  is  prob- 
ably to  be  regarded  as  a  mixed  infection  due  to  streptococci  or 
staphylococci.  Bauer  observed  a  post-scarlatinal  pericarditis  co- 
incident with  rheumatic  manifestations,  and  was  therefore  inclined 
to  attribute  it  to  the  affection  of  the  joints;  but  inasmuch  as  pus 
germs  are  often  responsible  for  the  rheumatic  affection,  the  peri- 
carditis, as  well  as  the  rheumatism  in  that  case,  may  very  well 
have  been  an  instance  of  mixed  infection  following  the  scarlatina. 

Other  Infections. — Other  diseases  in  the  course  of  whicli  acute 
pericarditis  has  occasionally  been  observed  are  erysipelas,  small- 
pox, tyjjhoid   fever,  measles,   cholera,   and  even  diphtheria.      It 


ACUTE   PERICARDITIS  4Y 

must  also  be  remembered  that  Flexner  found  as  foci  of  infection 
bronchitis,  leg  ulcer,  sloughing  myoma,  cancer  of  the  stomach,  and 
even  tonsillitis  and  disease  of  the  peritoneum.  In  some  it  was 
probably  a  secondary  event,  in  others  a  true  mixed  infection. 
When  pericarditis  complicates  acute  pleuritis  it  is  generally  stated 
to  be  by  extension.  It  is,  in  fact,  either  a  secondary  event  due  to 
the  one  and  the  same  cause,  or  it  is  a  mixed  infection. 

Acute  inflammation  of  the  pericardium  has  been  associated 
with  varying  diseases  of  neighbouring  parts — e.  g.,  enlarged 
glands  or  tumours  in  the  mediastinum,  abscess,  or  caries  of  a  rib, 
and  has  resulted  from  a  rupture  into  the  sac  of  an  empyema,  from 
perforation  from  an  ulcer  of  the  OBSophagus  or  stomach,  and  even 
from  intraperitoneal  abscess.  When  caused  by  such  conditions 
the  pericarditis  is  usually  purulent.  One  very  remarkable  case 
has  been  narrated  of  perforation  and  inflammation  of  the  pericar- 
dium by  a  set  of  false  teeth  which  had  been  accidentally  swal- 
lowed and  had  lodged  in  the  oesophagus,  where  it  caused  ulceration. 

Acute  pericarditis  is  sometimes  occasioned  by  aneurysm  of  the 
aorta  and  by  new  growths  in  the  pericardial  sac — e.  g.,  tubercles. 
These  are  capable  of  setting  up  an  acute  inflammatory  process  of 
the  pericardium,  but  as  a  rule  the  inflammation  is  subacute  or 
chronic,  which  probably  explains  why  it  so  frequently  escapes 
clinical  observation.  It  is  doubtful  whether  gummata  ever  in- 
duce acute  pericarditis. 

Haemorrhagic  pericarditis  occurs  as  a  secondary  infection  in  the 
course  of  scurvy,  purpura  hasmorrhagica,  and  haemophilia.  Some 
writers  also  assert  that  cancer  and  tuberculosis  induce  the  haem- 
orrhagic variety.  Ebstein  has  reported  two  cases  of  hiemorrhagic 
pericarditis,  and  stated  that  pericarditis  was  specially  likely  to 
be  haemorrhagic  in  the  chronic  or  recurring  form,  and  also  in  the 
aged  and  in  the  haemorrhagic  diathesis.  In  this  condition,  he 
thinks,  there  is  a  toxic  or  infectious  cause  that  creates  a  tendency 
to  haemorrhagic  exudates.  Such  changes  are  at  least  as  important 
as  the  mechanical  ones.  The  pericarditis  secondary  to  scorbutus 
may  be  regarded  as  a  type  of  this  class.  It  may  also  occur  in 
alcoholism,  which  induces  the  haemorrhagic  diathesis.  In  most 
cases  of  traumatic  pericarditis  the  blood  found  in  the  sac  comes 
from  the  bleeding  wound.  Cases  of  traumatic  origin  in  which  the 
pericardium  is  not  perforated  are  harder  to  understand. 


48  DISEASES  OF  THE   HEART 

Valvular  Defects. — Chronic  valvular  disease  seems  undoubt- 
edly to  predispose  to  pericardial  inflammation ;  tins  is  said  to  be 
particularly  the  case  with  aortic  insufficiency.  Why  valvular  le- 
sions should  thus  tend  to  the  production  of  pericarditis  is  a  mat- 
ter for  conjecture.  By  the  advocates  of  the  doctrine  of  the  infec- 
tious origin  of  all  inflammations,  it  would  probably  be  explained 
as  an  instance  of  secondary  or  mixed  infection,  in  consequence  of 
the  very  close  anatomical  and  physiological  connection  existing 
between  the  endocardium  and  pericardium. 

Trauma. — Finally,  acute  pericarditis  is  sometimes  the  result 
of  direct  injury,  as  gunshot  or  stab  wounds,  blows'  upon  the  chest- 
wall  and  laceration  by  fractured  ribs.  Under  such  circumstances 
micro-organisms  are  usually  introduced  into  the  pericardium,  and 
there  set  up  an  acute  inflammatory  process  which,  if  the  cocci  be 
pyogenic,  will  prove  to  be  suppurative. 

DRY   PERICARDITIS 

SvN. :  Fibrinous,  Plastic,  Adhesive  Pericarditis 

The  pathology  and  etiology  of  this  form  have  already  been 
consi(l(n-(Ml,  and  therefore  I  shall  pass  at  once  to 

Symptoms. — This  disease  usually  arises  during  the  course  of 
some  already  existing  infectious  process,  and  therefore  its  inva- 
sion, and  even  its  subsequent  progress,  are  likely  to  be  masked  for 
a  time  by  the  clinical  phenomena  of  the  primary  affection.  In- 
deed, some  authors  go  so  far  as  to  state  that  there  are  so  few 
subjective  symptoms  attending  dry  pericarditis  that  it  may  be 
said  to  be  a  latent  afi^ection.  In  many  instances  this  is  probably 
correct,  but  I  believe  the  existence  or  absence  of  subjective  phe- 
nomena is  determined  by  the  degree  of  intensity  and  extent  of  the 
pericardiiil  inflammation. 

If  in  the  course  of  acute  articular  rheumatism  there  is  a  sud- 
den elevation  of  temperature  which  cannot  ])e  explained  by  the 
fresh  involvement  of  other  joints,  or  if  (Icliriiiin  or  pronounced 
disturbance  of  the  nervous  system  suddenly  takes  place,  especially 
in  children,  it  is  suspicious  of  some  of  the  lieart-structures  having 
become  invaded  by  the  inflannnatory  ])rocess.  This  organ,  there- 
fore, should  at  once  be  carefully  examined,  and  if  necessary  re- 
peatedly examined,  for,  according  to  the  fig\ires  already  quoted 


DRY  PERICARDITIS  49 

from  Poynton,  the  pericardium  in  children  is  a  specially  frequent 
seat  of  inflammation.  If,  as  thought  by  Roberts,  the  opinion 
appears  to  be  quite  prevalent  among  general  practitioners  that 
acute  fibrinous  pericarditis  is  not  very  frequent  among  children, 
and  not  apt  to  leave  serious  consequences  behind,  it  certainly 
would  seem  to  be  in  place  to  again  call  attention  to  Poynton's 
figures.  Out  of  150  fatal  cases  of  rheumatic  heart-disease  in  chil- 
dren, there  was  evidence  of  more  or  less  acute  plastic  pericarditis 
in  all  but  9.  In  113  the  pericardium  was  more  or  less  adherent, 
while  in  11  the  adhesion  was  complete.  Moreover,  the  pericarditis 
appeared  to  contribute  more  to  the  fatal  issue  than  did  the  endo- 
carditis, for  the  reason  that  the  inflammatory  process  extended 
from  the  pericardium  to  the  myocardium  and  led  to  dangerous 
dilatation. 

Pain. — This  is  an  early  and  fairly  constant  symptom,  although 
in  some  cases  it  appears  to  be  more  like  a  vague  sense  of  distress 
than  actual  pain.  It  is  generally  felt  in  the  cardiac  region,  but 
may  be  located  in  the  epigastrium,  while  in  some  cases  it  radiates 
over  the  front  or  side  of  the  chest,  even  along  the  course  of  the 
brachial  plexus  into  the  arm.  In  a  case  of  this  kind  described  by 
Sibson  there  was  also  endocarditis.  Occasionally  it  is  experienced 
between  the  shoulders,  and  is  then  held  to  indicate  inflammation 
of  the  posterior  portion  of  the  sac.  Baumler  has  described  pain 
and  sensitiveness  on  the  side  of  the  larynx.  In  some  instances 
there  is  associated  with  the  pain  such  a  hypersesthesia  of  the  skin 
of  the  pra^cordia  as  to  make  percussion  of  the  heart  almost  impos- 
sible. Painful  deglutition  has  been  frequently  reported,  and  is 
not  difiicult  to  understand  when  we  remember  that  the  pericar- 
dium is  attached  to  the  oesophagus  and  would  be  pressed  upon 
by  the  ingesta  in  their  passage  down  the  gullet.  Patients  have 
also  been  known  to  complain  of  the  heart  hurting  them  with  each 
contraction,  and  it  may  well  be  that  when  the  covering  of  the 
heart  is  inflamed  pain  can  be  felt  every  time  the  organ  changes  in 
form  during  systole. 

In  character  and  severity  this  symptom  differs  much  in  differ- 
ent cases.  It  may  be  sharp  and  cutting  or  dull  and  heavy.  In  a 
case  observed  recently  the  patient  was  only  able  to  describe  his 
pain  as  a  steady  dull  ache  over  the  heart.  Usually  the  anguish  is 
continuous,  although  in  some  cases  it  is  intermittent,  coming  and 


60  DISEASES  OP  THE  HEART 

going  like  a  veritable  neuralgia.  In  others  again  it  assumes  a 
paroxysmal  character.  The  countenance  generally  betrays  suffer- 
ing by  an  expression  of  pain  or  distress,  and  the  patient  not  infre- 
quently keeps  his  hand  upon  his  heart.  Although  this  symptom, 
pain,  is  doubtless  due,  in  large  part  at  least,  to  the  friction  pro- 
duced by  the  rubbing  together  of  the  inflamed  pericardial  sur- 
faces, still  its  intensity  depends  also  upon  the  sensitiveness  of  the 
patient,  it  being  well  known  that  some  persons  never  feel  pain  so 
acutely  as  do  others  of  a  less  phlegmatic  temperament.  The  pain 
of  pericarditis  persists  so  long  as  the  inflamed  surfaces  continue 
to  rub  against  each  other,  and  hence  when  these  become  separated 
by  effused  fluid  this  symptom  abates  or  disappears.  Therefore,  if 
pain  suddenly  ceases  while  the  continuance  of  pyrexia  points  to 
continuance  of  the  active  inflammation,  it  may  be  taken  to  indi- 
cate beginning  effusion  into  the  sac. 

Cough  may  or  may  not  be  present,  but  when  present  is  usually 
dry  and  frequent,  and  when  conjoined  with  pain  may  give  rise  to 
the  suspicion  of  pleurisy.  In  a  fourteen-year-old  girl  seen  not  long 
ago  and  in  whom  the  inflamed  pericardium  had  led  to  great  car- 
diac dilatation,  with  consequent  pressure  on  the  left  lung,  the 
attending  physician  at  first  mistook  the  case  for  one  of  pneu- 
monia. This  case  is  so  instructive  that  I  will  briefly  rej^ort  its 
salient  features.  On  a  certain  Friday  this  girl  complained  of 
slight  pain  and  stiffness  of  one  of  her  legs,  but  was  not  prevented 
there])y  from  going  to  school  as  usual.  The  following  Monday  she 
felt  several  slight  chills,  which  were  attributed  to  the  coldness  of 
the  room  in  which  she  was  at  the  time.  For  several  days  follow- 
ing she  showed  signs  of  malaise,  and  in  other  respects  did  not 
seem  well,  yet  did  not  give  up  and  go  to  bed.  Friday  night,  a 
whole  week  from  her  initial  rheumatic  attack^  she  spent  at  a 
friend's  house,  but  when  the  next  morning  came  was  unmistakably 
ill,  and  the  family  doctor  was  sent  for.  He  found  her  with  a  dry 
cough,  hurried  respirations,  rapid  pulse,  considerable  fever,  and 
a  sharp  pain  in  the  left  side  above  the  heart.  Examining  tlie 
lungs,  and  discovering  some  dulness  and  bronchial  breathing  at 
the  left  posterior  base,  lie  pronounced  the  case  ])neumonia — an  error 
that  could  have  been  avoided  by  a  proper  examination  of  the  heart. 
Three  days  later  another  physician  saw  the  patient,  and  at  once 
recognised  the  true  character  of  the  disease.     When  on  the  ensu- 


DRY  PERICARDITIS  51 

ing  afternoon  I  was  called  in  consultation,  the  cardiac  dulness 
presented  the  characteristic  triangular  outline  and  a  systolic  apex- 
murmur  was  audible,  but  the  friction-sound  had  disappeared. 
The  case  was  one  of  acute  pericarditis,  as  shown  a  few  days  subse- 
quently by  the  results  of  aspiration.  The  amount  of  effusion  was 
small,  however,  and  the  marked  increase  in  the  area  of  cardiac 
dulness  was  due  chiefly  to  the  dilatation  the  heart  had  undergone. 
It  was  impossible  to  say  whether  the  mitral  systolic  murmur  indi- 
cated a  valvular  lesion  or  was  relative  in  consequence  of  the  dila- 
tation. But  as  there  was  a  history  of  some  sort  of  illness  three 
years  before,  at  which  time  she  had  "  heart  trouble,"  it  was  feared 
that  the  valves  were  defective  and  were  perhaps  sharing  in  the 
present  inflammation.  In  this  case  the  pericarditis  had  probably 
begun  almost  a  week  before  she  was  obliged  to  give  up,  so  that  it 
is  not  strange  that  the  process  should  have  induced  signs  of  pres- 
sure by  the  end  of  the  first  week.  This  patient  ultimately  made  a 
good  recovery.  ^ 

The  pulse  in  these  cases  is  accelerated,  running  sometimes  as 
high  as  130,  or  even  140  to  the  minute,  and  is  usualy  compres- 
sible and  regular  in  the  early  stage  before  the  myocardium  has 
become  much  affected. 

The  respirations  are  usually  rapid  and  often  shallow,  either 
because  the  patient  shrinks  from  taking  a  deep  breath,  lest  the 
pain  be  intensified,  or  because  an  actual  sense  of  dyspnoea  is  ex- 
perienced. 

Temperature. — An  elevation  of  body-temperature  probably  at- 
tends most  cases  of  acute  pericarditis,  but  is  often  masked  or  modi- 
fied by  the  fever  due  to  the  primary  affection.  As  a  rule,  the 
degree  of  pyrexia  is  not  great,  averaging  perhaps  102°  to  103°  F., 
and  being  generally  continuous  or  mildly  remittent.  When  it 
occurs  in  the  course  of  chronic  nephritis,  or  when  it  is  associated 
with  chronic  myocardial  or  endocardial  lesions  and  independent 
of  rheumatism,  the  pericarditis  frequently  runs  its  course  with- 
out fever,  or  at  all  events  with  so  slight  a  pyrexia  as  to  be  over- 
looked. The  duration  of  the  temperature  is  somewhat  variable, 
depending  on  the  intensity  of  the  infection,  but  may  be  said  to 
average  two  to  three  weeks. 

Loss  of  appetite  and  other  derangements  of  the  digestive  tract, 
as  flatulence  and  constipation,  are  usually  present,  the  same  as  in 


52  DISEASES  OF  THE  HEART 

other  febrile  and  acute  infectious  processes,  while  the  uriiie  is 
scanty  and  high-coloured.  If  it  contains  albumin,  this  is  due  to 
an  associated  nephritis  or  depends  either  upon  a  primary  affection 
or  upon  a  long-standing  visceral  engorgement  resulting  from  ante- 
cedent cardiac  disease  and  is  not  due  to  the  pericarditis  itself. 

Sleep  is  disturbed  or  prevented  altogether  by  the  pain  and 
nervousness  cai;sed  by  the  inflammation.  C/hildren  are  often  fret- 
ful and  restless.  The  countenance  is  pale  and  anxious  or  expres- 
sive of  suffering.  In  the  spring  of  11)01  I  treated  a  gentleman  of 
fifty-five  for  symptoms  of  failing  heart,  the  result  of  chronic  myo- 
carditis and  associated  vascular  and  renal  changes.  He  was  tak- 
ing a  course  of  Xauheim  baths  and  seemed  to  be  getting  on  very 
well,  when  I  left  town  for  a  few  days.  Upon  my  return  I  re- 
ceived word  that  he  v.^as  very  ill  and  in  much  pain.  I  found  Mr. 
H.  sitting  in  a  chair  looking  pale  and  drawn,  and  when  he  spoke 
it  was  with  a  hollow,  feeble  tone  of  voice.  This  was  Thursday 
afternoon.  He  stated  that  on  the  Tuesday  morning  preceding  he 
had  been  seized  with  a  dull,  heavy  pain  over  the  heart,  which  had 
not  left  him  for  a  moment  since.  He  had  not  slept  for  two  nights, 
and  could  not  lie  down  on  account  of  his  great  shortness  of  breath. 
The  pulse  was  106,  weak,  inclined  to  be  thready,  yet  regular. 
His  breathing  was  not  noticeably  disturbed  so  long  as  he  was 
quiet,  but  his  temperature  in  tlie  mouth  was  101.2°  F.  Suspect- 
ing pericarditis,  I  yet  purposely  reserved  my  investigation  of  the 
heart  for  the  last  and  Avent  over  the  lungs  carefully,  finding  noth- 
ing more  than  rides  of  hypostatic  congestion  at  the  posterior  bases. 
Coming  to  the  heart  I  could  detect  no  change  over  what  had  been 
discovered  at  my  last  visit,  the  Saturday  previous,  excepting  that 
the  tones  were  much  more  feeble.  The  area  of  dulness  did  not 
a])])(>ar  increased. 

I  was  about  to  give  up,  in  doubt  of  the  nature  of  tlio  troul)le, 
when  I  chanced  to  catch  in  a  circumscribed  location  over  the 
roots  of  the  great  vessels  at  the  left  of  the  sternum  a  soft  brush- 
ing iimi'imii-  tliat  had  not  been  there  at  any  of  my  exaiiiiiintioiis 
before.  This  murmur  was  systolic  and  short,  not  at  all  like  a 
pericardial  rub  in  rhythm,  but  u])on  ])ressing  firmly  with  the 
stethoscope  I  discovered  tliat  the  imirniur  entirely  disappeared. 
This  convinced  me  tliat  the  case  was  one  of  acute  pericarditis, 
and,  knowing  the  feebleness  of  the  degenerated  heart,  I  believed 


DRY  PERICARDITIS  53 

the  attack  would  prove  speedily  fatal.  A  mustard-plaster,  fol- 
lowed by  hot  fomentations,  was  ordered,  and  a  nurse  was  at  once 
secured.  At  my  next  visit,  four  hours  later,  the  pain  was  miti- 
gated somewhat,  but  the  patient's  condition  was  manifestly  worse. 
Strychnine,  ^\,  was  ordered  hypodermically  every  two  hours,  and 
in  addition  ^  of  morphine  with  atropine  was  injected.  I  left 
him,  feeling  that  the  night  was  to  prove  a  critical  one,  and  at  mid- 
night I  received  a  telephone  message  that  Mr.  H.  was  failing  rap- 
idly, his  breathing  being  very  laboured,  and  his  pulse  at  the  wrist 
too  rapid  and  thready  to  be  counted.  A  physician  living  close 
by  the  patient  was  sent  at  once  and  began  the  administration  of 
stimulants,  but  with  no  apparent  effect,  as  the  patient  died  two 
hours  later.  It  was  subsequently  stated  to  me  that  as  his  condi- 
tion grew  worse  the  pain  became  less.  Consciousness  was  re- 
tained to  the  last.  J^o  autopsy  was  held,  but  I  believe  that  effu- 
sion began  to  take  place,  which  relieved  the  pain  by  separating 
the  inflamed  surfaces,  and  at  the  same  time  overpowered  by  its 
pressure  the  degenerated  myocardium,  which  led  to  rapid 
asystolism. 

The  insidiousness  of  onset  yet  intensity  of  subsequent  sjanp- 
toms  are  well  shown  by  the  case  of  Mrs.  B.,  a  ISTorwegian,  aged 
twenty-eight,  who  consulted  me  in  April,  188 Y,  "  for  heart  trou- 
ble." Her  mother  had  died  of  rheumatic  heart-disease  under  my 
care,  and  her  younger  sister  had  mitral  regurgitation,  also  of  rheu- 
matic origin.  Six  years  previously,  after  the  birth  of  her  only 
child,  the  patient  had  articular  rheumatism  and  was  ailing  for  a 
year,  yet  had  not  had  symptoms  of  heart-disease  afterward.  In 
December,  1886,  she  had  rheumatism  in  right  knee,  both  elbows, 
and  left  shoulder.  Three  weeks  before  coming  to  me  she  had 
begun  to  suffer  from  prcecordial  pains,  dyspnoea,  and  palpitation, 
each  heart-beat  accompanied  by  pain,  which  was  increased  by  deep 
breathing  and  lying  down. 

Percussion  occasioned  pain,  the  pain  being  most  marked  over 
the  sternum  and  adjacent  left  intercostal  spaces,  from  the  second 
to  the  sixth,  particularly  in  the  third  and  fourth.  The  patient's 
face  was  dusky,  the  eyes  dull,  and  a  systolic  pulsation  was  visible 
and  palpable  in  the  pulmonic  area.  There  was  slight  epigastric 
pulsation,  and  the  pulse  was  regular  and  feeble.  The  apex-beat 
was  in  the  fifth  left  interspace,  somewhat  too  far  to  the  left,  quick, 


54  DISEASES  OP  THE  HEART 

and  accompanied  by  a  feeble  thrill.  Cardiac  dulness  was  in- 
creased in  all  directions,  and  in  the  mitral  area  there  was  a  loud, 
harsh  systolic  murmur  transmitted  to  the  back.  All  the  sounds, 
especially  the  pidmonic  second,  were  sharj^ly  accentuated,  and  over 
the  base  of  the  heart  was  a  triple  murmur  that  by  its  rhythm  and 
other  characters  was  plainly  a  pericardial  friction-rub. 

Excepting  retraction  of  their  anterior  margins  the  lungs  were 
negative.  Her  temperature  and  urine  were  normal.  The  diagno- 
sis was  mitral  insufficiency  of  rheumatic  origin,  and  acute  peri- 
carditis, probably  plastic,  and  also  rheumatic. 

Patient  was  sent  home  to  bed  and  a  blister  was  applied  to  the 
pra^cordium.  At  first,  after  rest  in  bed,  local  applications  and 
salicylate  of  soda,  the  j^atient's  condition  improved,  and  she  was 
allowed  to  get  up  at  the  end  of  ten  days.  In  a  few  days,  however, 
she  again  took  to  her  bed,  and  from  this  time  forward  her  symp- 
toms steadily  grew  worse.  Cough  became  very  troublesome,  with 
difficult  mucous  or  muco-sanguineous  expectoration,  and  there  were 
anorexia  and  constipation.  The  pulse  always  remained  at  120, 
and  as  it  failed  to  be  slowed  by  digitalis,  the  drug  was  discontin- 
ued. June  2d  there  was  a  sudden  attack  of  acute  rheumatism  in 
the  left  hand  and  wrist  with  substernal  pain,  and  temperature  rose 
to  102°  F.  Salicylate  of  soda  gave  prompt  relief  to  pain,  and  as 
the  urine  was  scanty  and  acid,  the  salicylate  was  discontinued  for 
the  bicarbonate  of  potash,  which  was  administered  until  the  urine 
became  alkaline.  June  6th,  at  2  a.  m.,  there  was  a  sudden  exacer- 
bation of  substernal  jDain  and  distress.  A  pericardial  friction- 
sound  now  developed  over  the  body  of  the  right  ventricle,  chiefly 
below  and  to  the  left  of  the  ensiform  ap2:)endix.  There  was  great 
epigastric  tenderness  and  interscapular  pain.  The  anterior  mar- 
gin of  the  left  lung  became  somewhat  more  retracted,  and  the  apex- 
beat  now  moved  nearer  to  the  left  anterior  axillary  line.  The 
patient  complained  much  of  pain  across  the  front  of  the  chest, 
along  the  lines  of  the  diaphragm,  from  the  right  inframamillary 
to  the  left  infra-axillary  region.  She  complained  bitterly  of  pain 
in  the  ])it  of  the  stomach,  and  suffered  with  nausea  and  vomiting. 
June  8th  found  ])atient  much  distressed  for  breath  and  unable  to 
retain  food.  Epigastric  pain  diminished,  but  condition  of  the 
heart  very  much  as  before.  Fever  was  102°  F.  at  8  r.  m.  Stimu- 
lants and  food  in  small  amounts  were  ordered.     At  11  i*.  m.  there 


DRY  PERICARDITIS  55 

were  sudden  defervescence,  and  profuse  perspiration  for  the  rest 
of  the  night.  June  9th  patient  orthopnccic,  pulse  138,  unequal, 
and  weak ;  pain  abated ;  but  patient  restless.  Examination  re- 
vealed dulness  of  left  base,  as  high  as  lower  angle  of  scapula.  Ex- 
pectoration scanty ;  cough  almost  impossible ;  passed  a  very  bad 
night;  opiates  given  freely.  June  10th,  summoned  hastily  at 
noon  to  see  patient.  Abdomen  very  distended  with  gas ;  breath 
very  short ;  heart  very  feeble ;  carminatives,  stimulants,  and 
enemata  ordered,  but  very  little  relief  obtained.  Death  at  Y.30 
r.  M.  Treatment  throughout  tonic,  supporting,  sedative,  and  anti- 
rheumatic. 

Autopsy  by  Dr.  Elbert  Wing  nineteen  hours  after  death.  The 
inner  surface  of  the  pericardium  was  covered  here  and  there  with 
loose  fibrous  threads,  which  presented  the  appearance  of  cor  villo- 
sum,  while  upon  both  the  anterior  and  posterior  surfaces  of  the 
heart  was  an  area  of  recent  pericarditis.  The  sac  contained  a 
small  amount  of  serous  effusion.  The  myocardium  showed 
changes  of  chronic  myocarditis,  probably  dating  from  the  time  of 
the  previous  attack  of  pericarditis.  The  mitral  valves  gave  evi- 
dence of  chronic  endocarditis  that  had  led  to  their  insufficiency, 
and  showed  also  the  effects  of  recent  endocarditis.  There  was 
acute  circumscribed  pleuritis  of  the  left  side  with  about  8  ounces 
of  sero-fibrinous  effusion.  In  the  right  pleural  cavity  were 
old  pleuritic  adhesions.  The  lungs  were  hypersemic  and  (Edema- 
tous. There  was  subacute  diaphragmatic  peritonitis,  also  sub- 
acute splenitis,  and  passive  congestion  of  the  liver.  Kidneys  and 
other  organs  were  negative. 

In  some  patients,  particularly  children  suffering  from  acute 
articular  rheumatism,  there  may  be  marked  symptoms  pointing  to 
profound  disturbance  of  the  nervous  system.  These  are  jactita- 
tions, subsultus  tendinum,  cerebral  excitement  and  restlessness, 
and  low  muttering  delirium. 

It  must  not  be  supposed  that  all  the  foregoing  symptoms  are 
of  a  necessity  present  in  any  one  case  of  acute  fibrinous  pericar- 
ditis, or  that  they  always  have  the  gravity  just  described.  In  one 
patient  pain  is  the  chief  complaint,  another  may  be  annoyed 
by  persistent  palpitations,  others  may  manifest  no  particular 
disturbance  either  of  the  heart  or  nervous  system.  Unless  the 
pericarditis  is  associated  with  inflammation  of  the  endocardium, 


56  DISEASES  OF  THE  HEART 

dyspnopa  is  not  likely  to  be  marked  iiulil  the  acute  inflammatory 
process  gives  place  to  extensive  etfusion.  Respiration  may  be 
accelerated,  but  there  is  not  actual  air-hunger. 

In  many  instances,  as  previously  stated,  this  affection  remains 
so  latent  that  if  the  physican  were  to  rely  for  its  detection  upon 
subjective  manifestations,  the  disease  would  surely  be  overlooked. 
For  this  reason  the  medical  attendant  should  make  daily  examina- 
tions of  the  heart  as  a  matter  of  routine  practice,  in  all  cases  of 
rheunuitic  fever  or  other  infectious  diseases  capable  of  lighting 
uj)  ])eri('ardial  inflannnation. 

Course  and  Termination. — If  an  acute  dry  pericarditis  is 
circumscribed,  the  plastic  exudate  not  involving  the  whole  sac,  the 
activity  of  the  process  may  speedily  subside,  and  all  evidence  of 
its  existence  disappear  in  the  course  of  a  few  days  or  a  week.  If, 
on  the  other  hand,  the  inflammation  is  intense,  and  involves  the 
myocardium,  or  if  the  plastic  exudate  is  poured  out  over  the  entire 
organ,  the  course  of  the  disease  may  extend  over  several  weeks. 
In  such  cases,  particularly  in  children  with  already  existing  valvu- 
lar disease,  death  is  not  unlikely,  or  if  the  patient  recovers,  he  is 
likely  to  be  left  with  a  damaged  heart. 

Acute  cardiac  dilatation  is  not  infrequent,  as  shown  by  Poyn- 
ton's  statistics.  Indeed,  all  clinical  observers  of  much  experience 
with  pericarditis  in  children  have  come  to  look  upon  dilatation 
of  the  heart  as  a  quite  general  result,  and  to  regard  its  occurrence 
with  considerable  apprehension.  The  extension  of  the  inflamma- 
tion to  the  myocardium  is  a  matter  of  grave  danger,  and  one  that 
is  likely  to  result  fatally.  If  flbrin  be  deposited  in  a  thick  layer 
over  the  entire  surface  of  the  dilated  organ,  it  may  act  as  a  me- 
chanical hindrance  to  the  subsequent  return  of  the  heart  to  normal 
size.  This  extensive  fibrinous  exudation  results,  furthermore,  in 
an  adherent  pericardium,  which  will  be  described  in  a  subsequent 
cha])ter. 

Physical  Signs. — T nspeciion. — From  the  very  nature  of 
acute  fibrinous  pericarditis  it  is  evident  that  no  information  of 
more  than  a  merely  negative  kind  can  be  derived  from  an  ocular 
examination  of  the  patient.  The  countenance  may  express  anxiety 
or  suffering,  and  inspection  of  the  chest  may  note  some  disturb- 
ance of  respiration  or  an  exaggerated  and  rapid  heart-beat;  but 
if  there  be  evidence  of  deranged  circulation  this  will  probably 


DRY   PERICARDITIS  57 

be  found  due  to  associated  cardiac  disease,  as  acute  endocarditis, 
myocarditis,  cardiac  dilatation,  or  a  chronic  valvular  defect. 

Palpation. — In  some  cases  the  hand,  or,  as  preferred  by  Rob- 
erts, the  tips  of  the  fingers,  laid  gently  on  the  prgecordium,  detects 
a  vibration  or  fremitus,  which  is  the  tactile  impression  produced 
by  those  conditions  that  give  rise  to  the  pericardial  friction-sounds 
subsequently  to  be  described.  If  felt  at  all,  this  fremitus  is  de- 
tected over  the  body  of  the  heart,  usually  in  the  second  or  third 
intercostal  space,  not  far  from  the  left  sternal  margin.  It  may, 
however,  in  rare  instances  be  detected  at  different  points  through- 
out the  pra^cordium.  Unfortunately  this  sign  is  not  often  present, 
but  when  it  exists,  it  conveys  the  impression  of  a  rubbing  or  grat- 
ing of  two  rough  surfaces,  a  sort  of  "  to-and-f ro  "  or  back-and-forth 
rub,  which  is  not  strictly  synchronous  with  cardiac  systole  and 
-diastole.  It  is  this  peculiar  gliding  character  of  the  friction- 
fremitus  which  readily  enables  one  to  distinguish  it  from  an  endo- 
cardial thrill.  Pressure  may  modify  the  intensity  of  this  fremi- 
tus: moderate  pressure  increasing,  forcible  pressure  diminishing 
-or  obliterating  it  altogether. 

Percussion. — In  this  form  of  pericardial  inflammation  the  out- 
line of  cardiac  dulness  may  only  be  affected  in  so  far  as  this  dis- 
•ease  leads  to  dilatation  of  the  heart ;  in  other  words,  percussion 
reveals  nothing  characteristic  of  plastic  pericarditis,  or  that  will 
be  of  material  service  in  arriving  at  a  diagnosis. 

Auscultation. — In  the  early  stage  of  acute  pericarditis  of 
whatever  form,  and  it  may  be  throughout  the  entire  course  of 
•dry  pericarditis,  auscultation  furnishes  for  the  most  part  our  only 
means  of  diagnosis.  ISTormally,  the  two  pericardial  surfaces  glide 
over  each  other  without  friction  and  noiselessly.  But  when  one 
or  both  of  them  have  become  roughened  by  fibrinous  exudation 
more  or  less  friction  of  movement  is  occasioned,  and  this  is  de- 
clared by  the  so-called  pericardial  friction-sound. 

Before  describing  this  in  detail,  it  may  be  well  to  state  that 
.a  pericardial  friction-sound  has  also  been  detected  independently 
of  pericarditis.  It  may  be  produced  by  the  milk-spots  usually 
found  on  the  inferior  surface  of  the  right  ventricle,  also  by  con- 
-cretions  (Bauer) ;  by  dryness  of  the  serous  surfaces  (Collin 
and  Walsh) ;  and  by  viscosity  of  the  pericardium  during  an  at- 
tack of  cholera  (Pleischl),  Nevertheless,  such  facts  do  not  viti- 
6 


58 


DISEASES  OF   THE  HEART 


ate  the  truth  of  the  statement  that  in  the  recognition  of  the  peri- 
cardial friction-sound  lies  onr  best  and  usually  our  onlv  reliable 
means  of  arriving  at  a  djagnosis. 

Location  of  the  Pericardial  Frictioiruiurniur. — As  this  exo- 
cardial  murmur,  as  it  is  called  in  contradistinction  to  endocardial 

murmurs  of  valvular  disease, 
is  often  very  circumscribed, 
it  is  important  to  know  where 
it  is  most  frequently  and  best 
heard.  This  is  generally 
over  the  body  of  the  heart 
at  the  origin  of  the  great 
arteries  upon  which  the  peri- 
cardium is  reflected,  or  in 
some  cases  upon  the  anterior 
surface  of  the  right  ventricle, 
very  rarely  at  the  aj^ex  of 
the  heart.  Consequently  this 
friction-sound  is  audible  at  the 
left  of  the  sternum  in  the  sec- 
ond, third,  and  fourth  left  in- 
tercostal spaces  in  the  same 
locality  as  that  in  which  friction-fremitus  is  commonly  felt  (Fig. 
14).  In  some  instances  of  extensive  pericarditis  it  is  heard  at 
scattered  points  or  throughout  the  pra^cordium. 

Rhythm  of  the  Friction-sound. — This  is  the  most  important 
feature  of  the  pericarditic  rul),  and  the  one  upon  which  depend- 
ence is  chiefly  placed  in  the  interpretation  of  its  nature.  It  is 
very  variable,  but  whatever  its  peculiarity  in  any  given  case,  it  is 
as  a  rule  not  limited  to  systole  and  diastole,  as  are  endocardial 
murmurs.  Instead  of  being  synchronous  with  either  the  first  or 
second  heart-sound,  or  bearing  a  definite  relation  to  these  tones, 
the  pericardial  rub  seems  to  overlap  them  or  to  occur  at  a  time  that 
is  wholly  independent  of  them.  Thus,  according  to  Skodr.  it  may 
accompany,  precede,  or  follow  the  heart-sounds  in  what  seems  to 
be  a  sort  of  hit-or-miss  fashion.  The  rhythm  is  very  difficult  to 
describe,  but  when  (nice  heard  in  a  typical  case  is  again  easily 
recognised.  In  most  instances  the  friction-murmur  is  composed 
of  either  two  or  tliree  parts,  and  when  of  but  two,  has  a  to-and-fro 


i4. —  L'.-LAi.     l^.MAIl't.N      "Ir      i'tlill  AlilllAL 

Friction  Sound  and  Fkemitvs. 


DRY  PERICARDITIS  59 

or  back-and-fortli  rhythm,  after  the  manner  of  a  double  aortic 
bruit,  but  distinguishable  from  this  by  its  time  and  quality.  The 
variability  in  the  rhythm  of  this  sound  is  owing  to  the  fact  that 
the  roughened  pericardial  surfaces  are  made  to  rub  against  each 
other  either  during  contraction  or  relaxation  of  the  auricles  or 
during  the  corresponding  phases  of  the  ventricles.  Therefore, 
when  this  friction-murmur  is  made  up  of  three  parts,  one  is  pre- 
systolic, produced  by  the  systole  of  the  auricles,  and  the  other  two, 
of  longer  duration,  fall  in  the  systole  and  diastole  of  the  ventricles. 
Very  infrequently,  according  to  Bauer,  each  side  of  the  heart  can 
produce  a  systolic  and  a  diastolic  rub  of  different  duration,  so  that 
each  heart-beat  may  be  accompanied  by  four  murmurs.  Very 
rarely  also  a  friction-murmur  is  synchronous  with  either  one  or 
the  other  heart-sounds,  and  when  this  is  the  case  its  duration  is 
greater  than  that  of  the  tone  it  accompanies,  a  circumstance  by 
which  its  true  character  can  generally  be  recognised.  If  in  such 
a  case  one  is  in  doubt  as  to  whether  the  murmur  is  exocardial  or 
endocardial,  he  can  generally  ascertain  its  nature  by  noting  the 
effect  of  pressure,  since  this  exerts  little  if  any  influence  upon 
valvular  murmurs.  Finally,  it  should  be  remembered  that  a  fric- 
tion-sound may  disappear  for  hours  together  and  then  again  be- 
come audible. 

Intensity  of  the  Friction-sound. — This  depends  upon  two  con- 
ditions :  ( 1 )  the  nature  of  the  exudate,  ( 2 )  the  force  of  cardiac 
contractions.  If  the  deposit  is  fresh  and  semifluid  and  the  car- 
diac action  feeble,  the  sound  of  the  rub  is  likely  to  be  indistinct. 
If,  on  the  other  hand,  the  fibrin  is  dry  and  uneven  and  the  heart  is 
beating  forcibly,  the  friction-sound  is  likely  to  be  loud. 

Quality,  of  the  Friction-sound. — This  differs  in  different  cases, 
depending  probably  upon  the  dryness  and  viscosity  of  the  fibrin. 
It  may  be  grating,  creaking  like  leather,  crackling  like  parchment 
or  like  the  crunching  of  dry  snow  beneath  the  heel,  etc.,  but  in 
my  experience  is  most  often  of  a  soft  brushing  quality,  very  dis- 
similar to  the  timbre  of  valvular  bruits. 

The  Effect  of  Pressure  on  the  Pericardial  Murmur. — It  is 
usually  found  that  pressure  with  the  stethoscope  modifies  this 
friction-sound  in  its  intensity  if  not  its  quality.  Gentle  pressure 
by  bringing  the  roughened  surfaces  closer  together  intensifies  it, 
while  firm  pressure  diminishes  or  obliterates  it  entirely.     It  is 


60  DISEASES   OP  THE   HEART 

sometimes  found  also  that  the  intensity  of  the  murmur  is  affected 
in  one  way  or  another  by  the  patient's  position,  being  louder  in 
the  erect,  weaker  in  the  recumbent  posture  or  the  reverse.  In 
some  cases  also  the  intensity  is  affected  by  respiration,  being 
louder  when  by  forced  inspiration  the  pericardial  layers  are 
brought  into  lirmer  apposition,  and  contrariwise  enfeebled  when 
separated  by  expiration.  The  reverse  of  this  has  been  observed, 
however. 

There  is  nothing  in  acute  pericarditis  per  se  to  cause  abnor- 
mal alteration  of  the  heart-sounds.  As  stated  by  Roberts,  either 
tone  may  be  obscured  by  an  unusually  loud  and  harsh  friction- 
murmur,  but  in  general  they  are  heard  through  the  murmur  in 
those  cases  in  which  they  happen  to  l)e  synchronous.  When  the 
inflammatory  process  has  invaded  the  myocardium  or  has  weak- 
ened it  through  dangerous  dilatation,  the  cardiac  sounds  are  likely 
to  become  feeble,  and  the  first  at  the  apex  may  be  more  or  less 
toneless,  but  there  is  nothing  in  this  peculiar  to  pericarditis. 
Stasis  in  the  pulmonary  system  is  evinced  among  other  things  by 
undue  accentuation  of  the  ])ulmonic  second  tone,  while  in  conse- 
quence of  the  feeble  discharging  power  of  the  left  ventricle  the 
aortic  second  sound  becomes  enfeebled. 

Diagnosis. — The  diagnosis  of  dry  pericarditis  is  not  as  a 
rule  attended  Avith  insuperable  difficulty.  In  cases  in  which  it 
is  latent  or  its  symptoms  are  masked  l)y  those  of  the  primary 
affection  it  may  be  easily  overlooked.  In  most  instances  its 
presence  is  declared  by  the  history  of  an  antecedent  or  associated 
rheumatism,  by  prsecordial  pain,  etc.,  and  by  the  character- 
istic rubbing  thrill  and  murnuir.  When  the  anamnesis  and  symp- 
tomatology are  negative,  reliance  must  be  placed  upon  the  auscul- 
tatory phenomena,  and  these  failing,  a  correct  diagnosis  is  hardly 
possible. 

Differential  Diagnosis.  —  This  concerns  acute  endocarditis, 
pleurisy,  and  pneumonia.  The  diagnosis  of  acute  endocarditis 
is  hardly  possible  unless  valvuhir  murmurs  and  other  definite 
changes  in  the  soun<ls  and  shape  of  the  heart  and  embolic  phenom- 
ena are  detected.  The  differentiation  of  endocardial  from  exocar- 
dial  murmurs  is  based  on  the  laws  concerning  the  latter  just  de- 
scribed, aiul  as  a  rule  is  not  particularly  ditHcult  if  due  attention 
is  paid  to  their  rhythm. 


DRY  PERICARDITIS  61 

In  acute  pleurisy  reliance  must  he  placed  upon  the  detection 
of  the  characteristic  pleuritic  rub,  and  the  possible  development 
of  pleuritic  effusion,  since  the  history  and  symptoms  of  a  left- 
sided  pleuritis  may  be  very  like  those  of  pericarditis.  A  point  of 
prime  importance  is  that  the  pleuritic  rub  ceases  when  the  breath 
is  held,  while  that  of  pericarditis  does  not. 

In  pneumonia  there  are  the  initial  chill,  the  higher  continu- 
ous fever,  painful  difficult  cough,  tenacious  rusty  sputum,  loss  of 
normal  pulse-respiration  ratio,  dulness  of  one  or  more  lobes,  crepi- 
tant rales,  and  bronchial  breathing,  and,  lastly,  the  termination 
by  crisis  after  five  to  seven  days. 

One  would  scarcely  think  that  aortic  aneurysm  would  be  mis- 
taken for  pericarditis,  and  yet  I  recall  two  instances  in  which 
such  was  the  case.  A  middle-aged  gentleman  once  consulted  me 
because  of  pain  in  the  upper  front  chest.  The  only  abnormal  sign 
was  a  faint  scratching  sound  in  the  region  of  the  great  vessels  not 
synchronous  with  either  heart-sound.  In  the  absence  of  other  find- 
ings, I  pronounced  in  favour  of  localized  pericarditis,  and  yet 
four  months  later  I  discovered  in  the  same  situation  a  well- 
marked  aneurysm.  The  second  instance  was  that  of  a  man  in 
Cook  County  Hospital  who  presented  a  to-and-fro  rubbing  mur- 
mur over  the  base  of  the  heart,  also  not  synchronizing  with  either 
cardiac  tone,  no  dulness,  no  pressure-symptoms,  and  the  necropsy 
disclosed  three  small  aneurysmal  sacs  surrounding  the  base  of  the 
aorta.  They  were  of  about  the  size  of  English  walnuts,  and  the 
swish  of  the  blood  as  it  entered  and  left  the  sacs  had  evidently 
occasioned  the  pseudo-pericardial  rub. 

Prognosis. — This  is  always  grave,  but  depends  upon  the  se- 
verity and  duration  of  the  attack.  In  children  with  articular 
rheumatism  an  acute  attack  of  pericarditis,  even  without  effusion, 
is  so  likely  to  set  up  dangerous  dilatation  of  all  the  cardiac  cavi- 
ties that  if  the  disease  is  protracted  there  is  imminent  danger  of  a 
fatal  issue.  Dangerous  Aveakness  on  the  part  of  the  myocardium 
is  shown  by  feebleness  and  muffling  of  the  first  sound  at  the  apex, 
diminution  of  the  aortic  second  sound,  and  by  a  thready  and  in- 
termittent pulse.  Great  derangement  on  the  part  of  the  nervous 
system  is  also  a  sign  of  danger,  even  though  the  life  of  the  patient 
be  not  immediately  threatened.  The  remote  prognosis  is  unfa- 
vourable,  since   acute   plastic   pericarditis   may   be   followed   by 


62  DISEASES  OF  THE  HEART 

effects  that  will  greatly  hamper  the  heart  in  the  future.  Firm 
adhesions  at  different  points  may  unite  the  two  layers  of  the 
pericardium,  which,  if  they  do  not  become  stretched,  may  ulti- 
mately lead  to  weakness  and  dilatation  of  the  right  ventricle 
(Broadbent),  or  the  sac  may  be  bound  down  to  the  heart  through- 
out, forming  what  is  known  as  synechia  pericardii,  the  baneful 
effects  of  which  will  be  described  in  a  subsequent  chapter.  Broad- 
bent  has  related  a  case  in  which  the  (edema  and  other  signs  of 
persistent  venous  engorgement  throughout  the  body  were  found 
due  to  fibrous  bands  which  had  partly  constricted  the  right  auri- 
cle and  led  to  total  obliteration  of  the  inferior  v6na  cava. 

Although  it  is  stated  that  the  plastic  exudate  may  sometimes 
be  absorbed,  this  is  a  very  remote  contingency,  and  should  never  be 
reckoned  upon  as  at  all  likely.  When  the  disease  is  complicated 
with  endocarditis,  pleurisy,  or  pneumonia,  or  when  it  occurs  in 
the  course  of  chronic  Bright's  disease,  the  prognosis  is  usually 
more  unfavourable  than  when  it  occurs  independently  or  in  the 
course  of  rheumatic  fever. 

The  mortality  of  fibrinous  pericarditis  is  not  generally  con- 
sidered very  great,  and  yet  a  study  of  the  150  fatal  cases  of  rheu- 
matic heart-disease  collected  by  Poynton  shows  the  erroneousness 
of  this  opinion.  In  34  of  his  cases  myocarditis  was  present  as 
secondary  to  pericarditis  and  death  seemed  due  to  the  effect  upon 
the  myocardium.  Even  when  the  inflammation  does  not  extend 
to  the  heart-muscle  the  heart  of  a  child  is  very  likely  to  undergo 
a  serious  degree  of  dilatation,  and  when  both  these  conditions  are 
combined  with  endocarditis  recovery  is  very  improbable.  This 
was  well  shown  in  the  case  of  the  ten-year-old  coloured  boy,  from 
whom  was  obtained  the  specimen  shown  in  Fig.  13,  A\Tien  seen 
for  the  first  and  only  time  a  few  days  prior  to  death,  this  boy  was 
sitting  up  ill  bed  on  account  of  difficulty  of  respiration  and  of  pain 
in  the  heart-region.  ITis  illness  had  begun  with  rheumatism  and 
lasted  ten  weeks,  and  he  had  become  strikingly  emaciated  and  his 
countenance  showed  marks  of  patient  suffering.  The  thorax  and 
abdomen  were  distended  from  just  below  the  clavicles  to  the  um- 
bilicus, were  unnaturally  broad  across  the  loins,  and  thus  filled 
out  presented  a  striking  contrast  to  the  thinness  and  smallness  of 
the  neck  and  extremities.  Breathing  was  extremely  rapid  and 
shallow,  and  as  evinced  by  the  i)ulse  the  heart's  action  was  also 


DRY  PERICARDITIS 


63 


rapid   and  feeble.      The   skin  was   dry   and   scaly   and   felt   hot, 
although  as  a  matter  of  fact  there  was  but  slight  fever. 

The  cardiac  impulse  was  very  feeble,  and  the  apex-beat  could 
not  be  clearly  defined.  Absolute  dulness  was  enormously  in- 
creased in  all  diameters,  reach- 
ing as  high  as  the  second  costal 
cartilages,  and  transversely 
from  at  least  2  inches  to  the 
right  of  the  sternum  far  be- 
yond the  left  nipple  almost 
to  the  anterior  axillary  line 
(Fig.  15).  This  gave  to  the 
dulness  a  pyramidal  shape 
closely  resembling  the  outline 
of  the  pericardium  distended 
wutli  fluid,  but  differing  from 
it  in  the  circumstance  that 
the  left  border  of  dulness  did 
not  pass  outside  the  limits  of 
cardiac  impulse.  The  heart- 
sounds  were  feeble,  and  all 
over  the  prgecordium  was  a  loud,  harsh  systolic  murmur,  having 
its  greatest  intensity  in  the  mitral  area  and  audible  throughout 
the  back  of  the  chest.  jSTo  pericardial  friction-rub  could  be  dis- 
tinguished, but  there  w^as  one  sound  that  at  first  was  quite  mis- 
leading. 

Beneath  the  right  clavicle,  and  therefore  in  proximity  to  the 
aortic  area,  was  a  double  blowing  sound,  having  a  to-and-fro 
rhythm  of  a  quality  very  like  a  harsh  double  endocardial  murmur. 
It  was  so  loud  as  to  obscure  the  heart-tones,  yet,  although  very 
rapid,  not  fast  enough  to  be  generated  in  the  heart,  and  moreover 
was  audible  over  the  back.  So  soon  as  these  differential  points 
had  been  noted  it  was  concluded  to  be  respiratory,  and  accordingly 
w^as  found  to  cease  so  soon  as  the  little  patient  held  his  breath. 
The  lung-margins  in  front  were  retracted  by  the  pressure  of  the 
large  heart ;  pulmonary  resonance  was  impaired  to  right  and  left 
of  the  heart,  as  well  as  at  the  posterior  base  of  the  left  lung. 
There  was  manifest  engorgement  of  the  liver  and  other  abdominal 
viscera,  but  there  was  no  oodema. 


Fig.  15.- 


-Absolute  Dulness  in  Case  of 
Acute  Pericarditis. 


64  DISEASES  OF  THE  HEART 

In  the  matter  of  diagnosis  it  was  not  so  easy  to  determine 
whether  effusion  was  present  or  whether  the  enormous  area  of 
dulness  was  due  to  dihitation,  as  it  might  at  first  seem  to 
be.  However,  by  carefully  comparing  the  left  lateral  limit  of 
dulness  with  the  feeble  cardiac  impulse  and  finding  that  they 
pretty  closely  agreed,  it  was  concluded  that  the  condition  was 
mainly  dilatation,  secondar}^  to  acute  pericarditis,  and  probably 
also  endocarditis,  with  i)erhaps  a  small  amount  of  effusion,  but 
certainly  not  enough  to  warrant  tapping  in  the  hope  of  relieving 
the  child's  dyspna'a.  The  hopelessness  of  the  prognosis  in  such 
a  state  of  affairs  was  justified  by  the  fatal  issue  about  a  week 
subsequently. 

The  autopsy  disclosed  acute  plastic  pericarditis,  without  effu- 
sion, acute  endocarditis,  and  fatty  degeneration  of  the  myocar- 
diimi,  and  death  was  probably  to  be  attributed  to  the  state  of  the 
heart-muscle. 

PERICARDITIS   WITH    EFFUSION 

Sero-fihritious. — As  already  stated,  a  sharp  dividing  line  be- 
tween fibrinous  and  sero-fibrinous  pericarditis  cannot  always  be 
drawn  pathologically,  because,  although  a  pericarditis  may  remain 
dry  throughout  its  course,  the  fibrinous  exudate  is  generally  united 
with  an  effusion  of  serum,  so  that  a  process  which  was  plastic  at 
first  may  afterward  be  characterized  by  an  effusion  of  a  large 
quantity  of  serum  within  the  pericardial  sac.  The  two  elements 
of  fibrin  and  serum  may  be  mixed  in  varying  proportions ;  in  one 
case  the  former  being  abundant,  while  in  another  the  fluid  may 
contain  but  an  insignificant  proportion  of  plastic  material.  The 
amount  of  effusion  in  any  given  case  varies  within  wide  limits; 
there  may  be  1  or  2  ounces,  or  the  sac  may  be  enormously  distended 
by  1,  2,  or  more  pints  (Fig.  16).  The  effusion  generally  takes 
place  gradually,  but  in  some  instances  occurs  with  such  rapidity 
that  the  sac  becomes  entirely  filled  in  twenty-four  hours  from  the 
onset  of  the  affection. 

Purulent. — In  this  variety  the  effused  fluid  is  composed 
chiefly  of  pus  with  but  little  fibrin,  and  contains  pyogenic  bacteria. 
In  rare  instances  the  micro-organisms  may  be  of  such  a  nature 
that  the  purulent  fluid  becomes  foetid,  and  the  disease  assumes  a 
very  grave  aspect  from  the  onset. 


PERICARDITIS  WITH   EFFUSION 


65 


Ilcemorrliagic. — Tliis  form  is  characterized  by  the  effusion  of 
blood  into  the  pericardial  sac  as  a  result  of  the  intensity  of  the 
process,  which  undermines  the  integrity  of  the  pericardial  blood- 
vessels. Or  a  sero-fibrinous  effu- 
sion may  become  deeply  blood- 
stained through  ha?morrhages 
from  minute  vessels. 

These  three  varieties  of  effu- 
sion may  be  looked  upon  as  differ- 
ent manifestations  of  one  and  the 
same  process,  having  the  same 
pathology,  and  differing  only  in 
the  etiology  and  intensity  of  the 
inflammation. 

Symptoms. — These  are  to  be 
divided,  according  to  the  stage  of 
the  process,  into  (1)  those  that  at- 
tend the  onset,  and  which  are 
chiefly  inflammatory  in  their  na- 
ture;  and  (2)  those  that  result 
from  mechanical  distention  of  the 
sac,  which  are,  therefore,  symp- 
toms of  pressure  on  the  heart  and 
neighbouring  viscera.  Further- 
more, the  three  kinds  of  effu- 
sion should  be  theoretically  distin- 
guished one  from  the  other  by  the 
severity  of  their  symptoms — that  is,  of  their  constitutional  effects ; 
as  a  matter  of  fact,  however,  there  is  often  nothing  in  the  symp- 
tomatology that  declares  the  nature  of  the  exudate. 

The  phenomena  attending  the  early  or  inflammatory  stage 
have  been  described  imder  Dry  Pericarditis,  and  therefore  we  may 
pass  at  once  to  the  consideration  of  the  symptoms  due  to  fluid 
accumulation  in  the  sac. 

As  effusion  takes  place  it  gradually  distends  the  sac  from 
below  upward,  and,  separating  the  roughened  and  inflamed  peri- 
cardial surfaces,  causes  a  cessation  of  the  pain  attending  the  onset 
of  the  affection.  The  fever  of  the  inflammatory  stage  still  per- 
sists, however,  as  may  also  the  cough.     With  distention  of  the 


Fig.  16.  —  Case  of  Pericarditis  in 
WHICH  THE  Sac  contained  3j^ 
Pounds  of  Fluid.    (Brarawell.) 


66  DISEASES   OF   THE   HEART 

sac,  the  symptoms  due  to  active  inflammation  gradually  merge 
into  and  are  subordinated  to  those  occasioned  by  pressure.  When 
the  amount  of  exudation  is  small,  symptoms  of  active  inflamma- 
tion may  still  predominate,  but  Avhen  it  completely  fills  the  sac, 
reaching,  it  may  be,  one  or  more  pints,  pressure-effects  assert  them- 
selves, and  may  even  become  dangerous. 

Children  impress  me  as  complaining  less  of  these  effects  than 
do  adults,  yet,  of  course,  individual  peculiarity  largely  determines 
the  amount  of  complaint  upon  the  part  of  the  patient.  I  have 
seen  children  with  an  enormously  distended  sac  who  yet  uttered 
no  word  of  complaint  and  whose  silent  suffering  was  truly  pa- 
thetic. They  are  usually  restless,  however,  and  display  fretful- 
ness  when  disturbed.  In  nu^ny  cases  their  patient  fortitude  as 
regards  sul)jcctive  symptoms  presents  striking  contrast  to  the 
objective  evidence  of  circulatory  and  respiratory  embarrass- 
ment. 

The  face  is  pale  and  anxious,  or  there  is  congestion  of  the 
cutaneous  vessels,  producing  a  blue-white  appearance,  and  the 
veins  of  the  neck  are  turgid.  The  pidse  is  small,  rapid,  and  of 
low  tension,  which  gives  it  a  degree  of  abruptness  that  may  make 
it  somewhat  resemble  the  sudden  pulse  of  aortic  incompetence. 
Some  writers  describe  the  pulse  in  the  stage  of  effusion  as  larger 
and  fuller  than  would  be  expected  from  the  feebleness  of  the  heart- 
soimds.  Marked  irregularity,  and  even  intermittence,  are  some- 
times observed,  particularly  after  the  effusion  has  persisted  for 
a  considerable  time.  Such  arrhythmia  coming  on  late  is  a  sign  of 
danger,  since  it  points  probably  to  failure  of  the  heart-muscle. 
It  should  not  be  forgotten,  however,  that  irregularity  and  inter- 
mittence of  the  pulse  may  be  present  from  the  beginning  of  the 
pericarditis,  when  this  latter  is  associated  Avith  a  valvular  defect, 
in  which  case  it  is  not  to  be  attributed  to  the  pericardial  effusion 
or  inflannuation. 

The  disturbance  of  the  circulation  everywhere  evinced  is  a 
direct  result  of  pressure  on  tlio  heart  by  the  abundant  effusion. 
Not  only  does  the  heart  have  to  sustain  the  weight  of  the  super- 
imposed fluid,  but  when  the  effusion  is  great  enough  to  distend 
tlie  sac,  it  is  confined  under  high  tension  and  forced,  therefore, 
to  press  inward  on  the  heart.  According  to  Sibson,  the  thick- 
walled  and  powerful  ventricles  are  better  able  to  withstand  such 


PERICARDITIS   WITH   EFFUSION  67 

pressure  than  are  the  thin-walled  auricles  and  veins,  which  con- 
sequently have  their  capacity  diminished.  There  is  actual  me- 
chanical impediment  to  the  inflow  of  blood  into  the  right  heart, 
and  likewise  to  passage  of  the  stream  out  of  the  pulmonary  veins 
into  the  left  auricle.  Thus  are  produced  the  smallness  and  weak- 
ness of  the  radial  pulse  with  fulness  of  the  systemic  veins. 

This  is  not  all  of  the  pressure-effects,  however.  The  distended 
pericardial  sac  takes  up  more  room  than  it  did  prior  to  the  effu- 
sion, and  consequently  it  exerts  pressure  on  the  adjacent  viscera. 
It  pushes  aside  the  elastic  lung-borders ;  and  as  the  heart  lies  more 
■  to  the  left  than  to  the  right  of  the  median  line,  it  is  the  left  lung 
that  feels  the  greater  pressure.  The  lower  lobe,  therefore,  is 
shoved  backward  to  make  room  for  the  distended  pericardium, 
consequently  the  patient  suffers  from  respiratory  embarrassment 
more  or  less  pronounced.  Xot  only  are  the  respirations  acceler- 
ated and  shallow,  but  the  patient  is  compelled  to  sit  up  in  bed  to 
breathe  (orthopnoea),  or  in  some  instances  to  lean  forward  with 
his  elbows  on  his  knees,  so  as  to  allow  of  as  much  gravitation  of 
the  sac  away  from  the  lungs  as  is  possible  under  the  circumstances. 
No  doubt  that  carbonic-acid  intoxication  residting  from  the  me- 
chanical impediment  to  respiration  also  plays  a  part  in  the  pro- 
duction of  dyspnoea. 

Insomnia  is  often  a  very  troublesome  symptom,  and  seems  to 
be  due  not  only  to  passive  cerebral  congestion,  but  also  to  the 
patient's  dyspncea,  which  renders  it  impossible  for  him  to  lie 
down,  or  speedily  arouses  him  when  so  fortunate  as  to  fall  into 
even  an  uneasy  sleep. 

There  is  usually  anorexia ;  not  only  has  the  patient  no  appe- 
tite, but  the  dyspnoea  and  dysphagia  render  the  taking  of  food 
difficult,  and  children  often  turn  away  from  it  when  proffered. 

The  urine  is  scanty,  the  abdomen  is  distended  both  from  re- 
tention of  gas  in  the  bowels  and  from  congestion  in  the  portal 
system.  The  liver  is  turgid  in  consequence  of  mechanical  inter- 
ference with  circulation  through  the  lungs,  and  is  more  or  less 
tender ;  there  may  be  constipation  or  small  frequent  w^atery  stools, 
because  of  serous  transudation  into  the  intestines  from  the  en- 
gorged vessels  within  their  walls.  I  have  always  looked  upon  this 
diarrhoea  as  IS^ature's  effort  to  unload  the  distended  vessels,  and 
therefore  as  a  very  valuable  therapeutic  hint.     If  the  disease  be 


68  DISEASES  OF  THE   HEART 

protracted,  and  venous  congestion  very  marked,  there  may  even  be 
some  oedema  of  the  lower  extremities. 

Fever  is  of  variable  intensity  and  character;  it  is  likely  to 
abate  somewhat  as  the  active  inflammatory  stage  passes  into  that 
of  effusion,  and  if  this  latter  stage  persists  for  some  weeks  the 
temperature  usually  returns  to  normal,  or  nearly  so. 

The  symptoms  of  pressure  as  above  described  usually  manifest 
themselves  gradually,  but  appear  suddenly  in  those  cases  in  which 
the  sac  becomes  rapidly  filled.  The  gravity  of  the  symptoms  usu- 
ally bears  a  direct  relation  to  the  amount  of  effusion.  When  this 
is  small,  but  2  or  3  ounces,  or  when  it  takes  place  insidiously  in 
the  course  of  cachectic  diseases,  symptoms  may  be  entirely  latent. 

When  the  pericardial  effusion  is  purulent,  the  gravity  of  the 
symptoms  depends  both  upon  the  amount  of  the  exudation  and 
the  kind  of  micro-organisms  concerned  in  the  process.  It  is  in 
this  form  that  the  sac  often  reaches  its  greatest  degree  of  disten- 
tion, and  since  the  degree  of  mechanical  interference  with  both 
circulation  and  respiration  accords  with  the  amount  of  effusion  it 
requires  no  further  comment. 

Scarcely  had  the  foregoing  been  penned  when  I  was  asked  to 
see  2  cases  of  acute  rheumatic  pericarditis  in  children,  which  illus- 
trated so  well  certain  features  of  similarity,  and  yet  of  contrast, 
that  I  have  decided  to  narrate  them  here.  A  girl  of  twelve  years, 
seen  with  Dr.  F.  S.  Johnson,  gave  the  history  of  a  severe  attack  of 
inflammatory  rheumatism  five  years  previously  involving  several 
joints,  but  the  heart  was  said  not  to  have  been  affected.  She  after- 
ward had  two  mild  rheumatic  attacks,  of  which  the  last  was  a 
year  ago.  During  the  past  summer  and  fall  the  patient  was 
thought  by  her  parents  to  have  been  remarkably  well.  About 
four  weeks  ago  she  had  an  attack  characterized  by  mild  fever, 
coated  tongue,  and  slight  jaundice,  but  no  distinct  rheumatic  symp- 
toms. Ten  days  ago  she  was  allowed  to  attend  the  opera  and  eat 
freely  of  candy,  after  which  the  symptoms  of  two  weeks  earlier 
returned  with  greater  intensity. 

When  Dr.  Johnson  assumed  charge  of  her  case  he  found  the 
patient  with  mild  intermittent  pyrexia,  ankles  and  knees  painful, 
but  not  red  or  puffy,  slight  pnecordial  pain,  great  nervousness, 
restlessness,  and  so  much  cutaneous  hyperrpsthesia,  as  well  as  pain, 
that  a  very  thorough  examination  of  the  chest  was  not  possible. 


PERICARDITIS  WITH   EFFUSION  69 

He  found  weak,  rapid,  but  regular  pulse,  120  to  130,  and  respira- 
tions of  60 ;  great  increase  of  both  absolute  and  relative  cardiac 
dulness,  particularly  upward  and  to  the  left ;  a  loud  systolic  mur- 
mur throughout  pra?cordium,  but  most  intense  at  apex,  together 
with  a  short  presystolic  murmur  limited  to  a  small  area  within 
and  above  the  apex-beat. 

The  apex-beat  was  in  fifth  space  outside  left  nipple,  heart- 
sounds  were  everywhere  audible,  pulmonic  second  banging  and 
split.  A  pericardial  friction-sound  existed  at  the  base,  over  right 
auricle.  Left  lung  was  compressed  and  the  liver  palpable  just 
above  the  level  of  the  umbilicus.  There  was  no  dropsy,  and  the 
urine  was  negative. 

The  case  was  regarded  as  one  of  acute  rheumatic  pericarditis 
supervening  upon  a  combined  mitral  lesion,  and  having  led  to 
great  general  dilatation  of  the  heart.  Three  days  later  tempera- 
ture was  102°  F.,  pulse  120  to  130,  but  regular,  and  respira- 
tions 60  to  80.  Patient  was  in  evident  distress,  complaining  of 
pain  in  the  heart  above  the  left  nipple.  She  also  had  great  diffi- 
culty in  swallowing.  A  -J^-  grain  of  morphine  gave  her  a  fairly 
comfortable  night,  and  the  morning  when  I  saw  her  the  condition 
was  as  follows:  Patient  lay  nearly  flat  in  bed,  several  joints  of 
both  lower  and  upper  extremities  anointed  with  a  liniment  con- 
taining oil  of  wintergreen  and  swathed  in  bandages.  She  was 
excitable,  fretful,  and  inclined  to  cry  out  when  touched.  There 
was  no  cyanosis,  but  respirations  were  shallow  and  rapid,  60  or  80 
to  the  minute,  the  pulse  of  fair  volume,  but  dicrotic,  was  about 
120,  perfectly  regular.  The  abdomen  was  distended  and  tym- 
panitic, tense  and  painful  in  the  region  of  the  liver,  which  could 
be  made  out  extending  nearly  to  the  level  of  the  umbilicus.  The 
heart's  apex  was  visible  and  palpable,  though  rather  weak  and 
diffused,  in  the  fifth  left  interspace  outside  the  nipple-line.  There 
was  no  pericardial  fremitus,  but  the  cardiac  impulse  was  diffused 
from  apex  to  base  and  from  left  mamillary  line  to  the  sternum. 

Cardiac  dulness,  both  superficial  and  deep,  was  increased 
transversely,  but  chiefly  to  the  left,  the  deep  limit  reaching  nearly 
to  the  anterior  axillary  line,  but  not  extending  outside  of  or  be- 
low the  palpable  impulse  of  the  apex.  A  harsh  mitral  systolic 
murmur  was  everywhere  audible,  as  were  also  both  sounds,  the 
pulmonic  second  being  greatly  intensified  and  split.      Over  the 


70  DISEASES   OF   THE   HEART 

body  of  the  sternum  pressure  Avith  the  stethoscope  brought  out  a 
soft  rubbing  murmur,  which,  from  its  quality  and  rhythm,  was 
easily  recognisable  as  pericardial.  The  inferior  boundary  of  car- 
diac dulness  was  not  dei)ressed ;  indeed  the  abdominal  distention 
occasioned  an  eleyation  of  the  heart. 

This  high  position  of  the  liver  caused  the  upper  margin  of 
hepatic  dulness  to  reach  the  level  of  the  fifth  right  costal  cartilage 
and  interfered  with  the  detennination  of  the  presence  or  absence 
of  notch's  sign.  It  seemed  to  me,  however,  that  the  outer  border 
of  the  right  auricle  lacked  its  natural  curve  downward  and  inward, 
and  that  the  line  of  dulness  joined  that  of  the  liver  at  nearly  a 
right  angle.  Tlie  i)ain  which  change  of  position  caused  the  little 
patient,  rendered  examination  of  the  back  of  the  chest  inadvisable. 
The  doctor  stated,  however,  that  the  day  before  he  had  found  dul- 
ness with  corresponding  alteration  in  the  breath-sounds  at  the  left 
posterior  base. 

The  diagnosis  was  acute  rheumatic  pericarditis  with  great 
cardiac  dilatation  and  possible  acute  myocarditis  supervening 
upon  a  previously  existing  endocarditis  that  had  led  to  mitral  in- 
sufficiency. Distinct  signs  of  effusion  were  not  obtainable,  and 
hence  it  was  conclud(>d  that  the  exudate  was  fibrinous,  or  if  united 
with  serum,  the  proportion  of  the  latter  was  not  large.  The  ex- 
tensive dilatation  present  was  attributed  in  part  to  the  mitral 
lesion,  and  in  part  to  the  dilating  influence  of  the  pericarditis, 
Avhether  associated  with  acute  myocarditis  or  not. 

The  symptoms  in  this  case  were  not  distinctly  those  of  pres- 
sure;  respiration  was  greatly  accelerated,  to  be  sure,  but  there 
was  no  cyanosis,  no  downward  displacement  of  the  liver,  and  no 
orthopncea;  in  short,  the  symjitoms  pointed  more  to  disturbance 
of  the  nervous  system,  with  consequent  rapidity  of  breathing,  than 
to  circulatory  embarrassment.  The  very  considerable  hepatic  en- 
gorgement could  be  very  reasonably  referred  to  the  free  mitral 
leak  and  the  greatly  overstrained  right  ventricle.  This  patient 
ultimately  made  a  good  recovery. 

On  the  same  day  on  which  I  saw  the  preceding  patient.  Dr.  Jo- 
sephson  asked  me  to  visit  a  little  girl  of  six,  who  was  also  suffer- 
ing from  acute  pericarditis.  She  had  ])assed  through  an  attack 
of  scarlatina  in  the  Jnly  preceding,  and  for  the  past  three  or  four 
weeks  had  been  suffering  from  acute  articular  rheumatism,  which 


PERICARDITIS   WITH   EFFUSION 


71 


was  still  present  when  slie  came  nnder  the  doctor's  charge  eight 
days  before  my  visit.  lie  had  at  once  recognised  an  acute  inflam- 
matory affection  of  the  heart.  Her  somewhat  fluctuating  tempera- 
ture had  averaged  about  102°  F. 

The  child's  condition  when  I  saw  her  was  as  follows:  She  was 
sitting  in  bed,  not  even  venturing  to  rest  against  the  pillows, 
breathing  60  or  more  times  to  the  minute,  and  during  the  forenoon 
of  that  day  her  respirations  had  actually  been  90  to  the  minute. 
The  pulse  was  very  rapid,  small,  and  dicrotic,  but  perfectly  regu- 
lar. The  expression  one  of  patient  sufi^ering.  Upon  removal  of 
the  clothing  the  skin  was  found  hot,  dry,  and  scaly,  yet  broke 
out  into  a  perspiration  a  few  minutes  afterward  upon  the  child 

There  was  every  evidence  of  capillary 
The 


making  a  little  exertion 
and  venous  congestion. 
abdomen  M'as  distended  and 
hard,  particularly  about  the 
waist-line ;  the  thorax  was  evi- 
dently distended  to  its  utmost 
capacity,  the  entire  front  of 
the  chest  bulging,  and  the  in- 
tercostal spaces  more  or  less 
smoothed  out.  The  apex-beat 
was  feebly  palpable  below  and 
a  little  to  the  left  of  the  nip- 
ple, and  there  was  diffused 
systolic  shock  over  the  body  of 
the  organ.  Absolute  cardiac 
flatness  (Fig.  17)  began  at  the 
right  nipple,  passed  upward 
to  the  first  interspace,  then 
downward  and  outward  into  the  left  axillary  region,  well  outside 
of  the  visible  and  palpable  apex-beat.  Its  lower  boundary  reached 
at  least  to  the  eighth  costal  cartilage,  and  the  distended  sac  could  be 
felt  in  the  epigastrium.  A  rough,  blowing  systolic  murmur  was 
very  loud  in  the  mitral  area  to  the  left,  while  the  heart-sounds  were 
loud  over  the  base  of  the  organ,  the  pulmonic  second  being  very 
banging  and  slightly  split.  From  the  middle  of  the  sternum  down- 
ward to  the  ensiform  was  a  grating  pericardial  friction-sound, 
which  had  a  simple  to-and-fro  rhythm  not  synchronous  with  either 


17. — Absiiute    Dii.m;--.    i   ase    of 
Pericarditis  with  Effusion. 


T2  DISEASES   OF   THE   HEART 

systole  or  diastole.  At  the  left  base,  posteriorly,  was  a  dull  patch 
corresponding  with  Ewart's  dull  patch  in  outline,  but  the  harsh, 
very  hurried  breath-sounds  were  everywhere  audible.  In  front, 
resonance  was  impaired  beneath  both  clavicles,  and  the  sense  of 
resistance  imparted  to  the  finger  upon  percussion  of  the  prsscor- 
dium  was  remarkably  intense. 

In  this  case  the  diagnosis  was  also  acute  pericarditis,  but, 
unlike  the  foregoing,  there  was  a  massive  exudate,  occasioning 
very  grave  pressure-signs.  There  was  also  present  the  same  valvu- 
lar lesion,  mitral  regurgitation,  but  there  was  very  strong  suspi- 
cion of  the  existence  of  acute  endocarditis,  since  from  the  history 
of  scarlet  fever  in  July,  with  more  or  less  rheumatism  subse- 
quently, with  no  other  previous  etiological  factor,  it  was  not  likely 
that  the  mitral  disease  dated  back  more  than  six  months. 

Deglutition  gave  this  little  sufferer  so  much  distress  that  she 
would  hesitate  for  minutes  together  before  making  up  her  mind  to 
take  the  proffered  medicine  or  nourishment.  In  this  case  the 
urgency  of  the  symptoms  arose  from  pressure.  Dyspnoea  was  so 
great  that  the  little  thing  begged  to  be  allowed  to  stand  up,  evi- 
dently to  relieve  the  thoracic  organs,  already  much  compressed, 
from  still  greater  pressure  by  the  abdominal  viscera  forced  upward 
against  the  diaphragm  in  the  sitting  position. 

The  contrast  presented  by  these  two  cases  was  most  instructive. 
In  this  latter  case  paracentesis  pericardii  was  advised  without 
delay.  It  would  have  been  cruel,  if  not  useless,  to  postpone  the 
operation  until  trial  had  been  made  of  cathartics  and  diuretics. 
Far  better  tap  first,  and  administer  these  afterward. 

Suppurative  pericarditis  generally  occasions  ])honomena  of 
sepsis,  but  chills,  fever,  and  sweating  are  sometimes  said  to  be 
absent  (Koberts).  When  present  they  are  an  indication  of  sepsis, 
and  as  such  may  be  a  part  of  the  symptomatology  of  the  primary 
affection  as  well  as  of  the  pericarditis.  When  the  effusion  is  foetid, 
as  rarely  happens,  septic  symptoms  are  most  marked,  and  pros- 
tration comes  on  early  and  is  extreme.  In  some  cases  there  is 
nothing  in  the  nature  of  the  sym]>toms  whoreby  one  may  deter- 
mine the  purulent  character  of  the  exudate. 

The  symptomatology  of  hwrnorrliagic  ])(M-ioarditis  depends 
upon  the  rapidity  with  wliicli  the  eftiision  takes  ])lacc,  rather  than 
upon  its  nature.     A  lia-iiKirrhngic  cff'usion  into  the  pericardial  sac 


PERICARDITIS  WITH   EFFUSION  73 

during  the  course  of  scorbutus,  for  example,  may  take  place  so 
suddenly  that  symptoms  of  pressure  aud  of  anaemia  rapidly  de- 
velop. In  other  cases  the  effusion  is  slowly  produced,  and  symp- 
toms manifest  themselves  gradually  or  are  entirely  absent. 

In  Ebstein's  two  cases  the  symptoms  were  those  of  pressure, 
cyanosis,  dyspnoea,  cough,  and  pain,  but  in  one  the  condition  was 
thought  to  be  extreme  cardiac  dilatation,  and  its  true  nature  was 
not  recognised  until  at  the  autopsy.  Although  in  the  second  case 
pericardial  effusion  was  recognised  during  life,  there  was  nothing 
in  the  symptoms  to  point  to  the  h?emorrhagic  character  of  the 
exudate. 

Course  and  Termination. — There  is  no  uniformity  in  the 
clinical  history  of  pericarditis  with  effusion.  Cases  vary  widely 
from  each  other  in  the  mode  of  onset,  in  the  course  they  pursue, 
and  in  their  mode  of  termination.  An  ordinary  case  occurring 
during  a  rheumatic  attack  may  be  expected  to  terminate  by  absorp- 
tion in  two  to  four  weeks ;  this  happy  event  may  very  rarely  take 
place  within  a  few  days,  the  disease  having  passed  through  the  suc- 
cessive stages  of  inflammation,  effusion,  and  absorption  in  less 
than  a  week.  In  other  instances  the  affection  manifests  a  strong 
tendency  to  become  either  subacute  or  chronic.  While  in  others, 
again,  the  disease  is  characterized  by  phases  of  partial  absorption 
and  improvement,  which  are  each  in  turn  followed  by  a  recurrence 
of  inflammation  and  increased  effusion  (Bauer),  until  at  length 
the  patient  is  worn  out  by  the  persistent  and  obstinate  nature  of 
the  disease.  These  variations  depend,  no  doubt,  upon  the  activity 
of  the  etiological  agent,  and  are  not  at  all  surprising,  for,  as  every 
one  knows,  no  disease  presents  uniformity  in  its  clinical  phenomena. 

Other  conditions  besides  the  activity  of  the  pathogenic  agent 
also  determine  the  course  and  severity  of  an  acute  pericarditis. 
Its  occurrence  with  or  as  a  sequel  to  pleurisy  or  pneumonia  is 
also  likely  to  influence  its  course  and  termination,  in  accordance 
with  the  intensity  of  these  latter  processes  and  the  degree  to  which 
they  have  undermined  the  patient's  resistance.  When  pericarditis 
is  the  result  of  chronic  nephritis  it  is  very  likely  to  run  a  slow  and 
latent  course. 

In  children  with  inflammatory  rheumatism  the  disease  is  apt 
to  prove  persistent,  and  if  it  does  not  destroy  life  by  invading  the 
myocardium,  terminates  in  complete  or  partial  synechia  pericardii. 


74  DISEASES  OF  THE  HEART 

Suppurative  pericarditis  is  a  very  serioiTS  affection,  manifest- 
ing but  little  tendency  to  spontaneous  recovery.  It  is  stated,  how- 
ever, that  if  the  pyogenic  bacteria  be  not  very  virulent,  and  if  life 
be  prolonged  for  a  considerable  time  beyond  the  stage  of  active 
inflammation,  absorption  of  the  more  liquid  portion  of  the  exu- 
date may  take  place,  the  residue  becoming  cheesy  and  in  time  in- 
filtrated with  lime-salts.  They  are  eventually  transformed  into 
calcareous  plates,  which  may  even  be  so  extensive  as  to  inclose 
the  heart  in  a  case  of  bone-like  hardness.  I  have  observed  two 
such  cases ;  in  one  a  calcareous  plate  the  size  of  a  silver  dollar 
was  found  on  the  anterior  surface  of  the  left  ventricle,  while  in 
the  other,  masses  of  lime  completely  surrounded  the  organ.  This 
latter  case  will  be  described  in  the  article  on  Adherent  Pericar- 
dium. Most  cases  of  purulent  pericarditis,  unless  relieved  by  sur- 
gical interference,  pursue  a  rapid  course,  and  jDatients  succumb 
more  or  less  speedily  to  the  etTects  of  py?emia,  resulting  either 
from  the  pericardial  or  primary  affection. 

In  the  form  of  ha?morrhagic  pericarditis,  which  occurs  in  the 
course  of  scurvy  and  is  observed  in  the  maritime  provinces  of 
Russia,  the  effusion  often  takes  place  with  great  rapidity  and 
destroys  life  in  one  or  two  days.  In  these  cases  death  seems  due 
in  no  small  measure  to  the  rapidly  induced  anaemia. 

Finally,  the  course  of  acute  pericarditis  with  effusion  is  deter- 
mined not  alone  by  the  intensity  of  the  inflammation,  but  by  the 
amount  of  the  exudation.  If  this  is  sufficient  to  greatly  distend 
the  sac,  its  absorption  is  hindered  by  the  tension  thus  occasioned. 
In  some  instances,  no  doubt,  a  pericardial  exudation  is  absorbed, 
and  no  permanent  ill  effects  remain. 

Physical  Signs. — Inspection. — The  degree  of  information 
afforded  by  insj)cction  depends  upon  the  amount  of  effusion  and 
the  conditions  residing  in  the  chest-walls.  In  a  child  of  tender 
age  or  a  person  with  a  yielding  chest-wall  a  comparatively  small 
pericardial  effusion  may  occasion  perceptible  prominence  of  the 
praecordium,  while  if  the  thorax  is  voluminous,  and  the  costal  car- 
tilages have  become  hard  and  inelastic  from  age,  it  is  possible  for 
even  an  enormously  distended  sac  to  produce  no  visible  bulging  of 
the  cardiac  area.  As  a  rule,  however,  more  or  less  prominence  in 
this  region  is  observed,  wliilo  the  intercostal  spaces  look  filled  out, 
and  the  skin  covering  them  appears  tense  and  shiny.     The  apex- 


PERICARDITIS  WITH   EFFUSION  Y5 

beat  is  not  visible,  or  but  faintly  so,  and  cardiac  impulse  is  feebly 
diffused  or  wanting.  The  apex-beat,  moreover,  if  visible,  may  be 
situated  lower  than  normal  when  the  liver  is  depressed  by  a  mas- 
sive effusion,  and  in  such  a  case  there  may  be  bulging  of  the  epi- 
gastrium. 

Cyanosis  and  distended  veins  give  evidence  of  circulatory  dis- 
turbance, while  respiratory  embarrassment  is  evinced  by  hurried 
breathing  and  restricted  movements  of  the  chest.  If  copious  effu- 
sion occasions  great  ]3ressure,  and  particularly  if  this  has  formed 
rapidly,  the  attitude  of  the  patient  and  the  expression  of  his  coun- 
tenance betray  suffering  and  it  may  be  oppression. 

Inspection  is  an  aid  to  diagnosis,  but  cannot  solely  be  relied 
upon,  since  precordial  bulging  in  children  may  be  the  result  of 
cardiac  enlargement  without  pericarditis. 

Palpation. — In  great  effusion  the  roughened  pericardial  sur- 
faces are  removed  from  each  other,  and  hence  the  hand  no  longer 
detects  the  peculiar  fremitus  present  in  the  beginning  of  the  pro- 
cess, when  the  exudate  is  fibrinous  and  not  serous. 

Otherwise  paljDation  serves  chiefly  to  corroborate  the  result  of 
inspection.  The  prsecordial  area  may  impart  a  sense  of  increased 
resistance  from  internal  pressure,  and  the  normal  intercostal  de- 
pressions are  found  obliterated.  Rarely  there  is  fluctuation.  In- 
creased resistance  and  tension  may  also  be  detected  in  the  epigas- 
trium. Older  writers  were  accustomed  to  attach  great  importance 
to  an  elevation  of  the  apex-beat,  which  they  explained  by  lifting 
of  the  apex  of  the  heart  by  the  effused  liquid.  Roberts,  Ewart, 
and  others  regard  this  as  erroneous,  believing  that  w^hat  was 
thought  to  be  the  apex-beat  is,  in  fact,  the  impulse  of  the  body  of 
the  heart  as  it  is  thrown  against  the  anterior  chest-wall  by  the 
collection  of  fluid  behind,  the  apex  of  the  organ  being  at  the  same 
time  moved  backward  and  to  the  left.  In  cases  of  extreme  effu- 
sion the  depression  of  the  diaphragTn,  occasioned  by  the  heavy  sac, 
leads  to  an  actual  lowering  of  the  apex-beat  (Bauer).  The  peri- 
cardial fremitus  present  during  the  inflammatory  stage  disappears 
with  the  occurrence  of  effusion.  In  some  cases  the  head  of  the 
left  clavicle  is  said  by  Ewart  to  be  elevated  so  that  the  first  rib 
can  be  felt  all  the  way  to  the  sternum  ("  first-rib  sign  "). 

The  most  striking  character  of  the  pulse  is  its  want  of  tension. 
It  is  rapid  and  may  be  regular  or  irregular,  even  intermittent.    In 


76  DISEASES  OF   THE   HEART 

some  instances  pulsus  paradoxus  is  present.  This  is  an  inversion 
of  what  is  usually  observed  during  the  two  acts  of  inspiration  and 
expiration.  Instead  of  becoming  stronger  and  fuller  at  the  end 
of  inspiration  and  the  beginning  of  expiration  the  pulse  becomes 
small  and  weak,  or  may  even  disappear  during  deep  inspiration, 
becoming  again  stronger  and  fuller  toward  the  end  of  expiration 
and  the  beginning  of  the  next  ensuing  inspiration.  Pulsus  para- 
doxus is  inconstant  and  is  not  pathognomonic  when  present,  and 
possesses  therefore  only  a  negative  value. 

Percussion. — This  method  of  investigation  furnishes  the  only 
reliable  sign  of  pericardial  effusion,  since  by  this  means  one  is 
often  able  to  determine  the  presence  of  so  small  an  amount  as  100 
cubic  centimetres  (Bauer),  150  to  ^00  cubic  centimetres  (Aparti 
and  Figaroli).  That  one  may  understand  why  so  much  reliance 
is  to  be  placed  upon  percussion,  I  will  consider  for  a  few  moments 
in  what  way  pericardial  effusion  alters  the  normal  relation  of  the 
parts  and  modifies  the  area  of  cardiac  dulness. 

The  pericardium  is  a  closed  sac,  which  is  thrown  around  the 
heart,  being  wrapped  about  the  origin  of  the  great  vessels  above, 
and  attached  to  the  central  tendon  of  the  diaphragm  below.  When 
fluid  is  effused  into  this  closed  cavity  it  sinks  to  the  most  depend- 
ent part,  and  then  creeping  upward  distends  the  sac  in  all  direc- 
tions, pushing  aside  the  anteri(U'  borders  of  the  overlapping  lungs. 
The  area  of  absolute  cardiac  dulness  now  becomes  altered  in  a 
striking  manner  (Fig.  17),  and  to  an  extent  commensurate  with 
the  amount  of  effusion.  Some  authorities  consider  that  this  alter- 
ation of  cardiac  dulness  corresponds  in  shape  with  that  of  the  dis- 
tended sac  (Bauer,  Sibson),  while  others  attribute  it  chiefly  to 
the  crowding  aside  of  the  lung-nuirgins  (Duchex,  Rotch).  My 
own  opinion  is  that  the  configuration  of  this  area  depends  largely 
upon  the  anatomical  arrangement  of  the  lung-borders  overlapping 
the  heart,  since  when  they  become  retracted  by  adhesions  and  in 
cardiac  dilatation,  the  shape  of  the  resulting  dulness  is  essentially 
the  same,  though  less  extensive,  as  in  pericarditis  with  effusion. 
Probably  both  factors,  the  sha])e  of  the  sac  and  the  arrangement 
of  the  lung-l)orders,  are  responsible  for  the  peculiar  outline  of  the 
area  of  dulness  observed.  This  area  of  absolute  dulness  or  flat- 
ness is  variously  described  as  triangular,  pyramidal,  pear-shaped, 
or  pyriform,  that  of  a  truncated  cone,  or  ''  that  of  a  bag  of  fluid 


PERICARDITIS  WITH  EFFUSION  77 

spreading  out  at  the  base"'  (Ewart).  Its  broad  base  rests  upon 
the  diaphragm,  while  its  rounded  apex  occupies  the  upper  sternal 
region.  A  glance  at  Fig.  17  shows  that  the  direction  of  the  two 
side-lines  is  not  the  same,  being  rather  more  vertical  at  the  right. 
The  right  arm  of  this  irregular  triangle  is  shorter  and  straighter, 
while  the  upper  or  left  boundary  presents  an  indentation  or  con- 
cavity soon  after  leaving  the  apex,  and,  sloping  gradually  down- 
ward, joins  the  base-line  at  a  rounded  somewhat  obtuse  angle. 

The  shape  of  this  area  is  by  most  authors  considered  very  char- 
acteristic, although  Shattuck  is  of  the  opinion  that  the  peculiar 
feature  is  not  the  form,  but  the  fact  that  the  dulness  spreads  out  in 
all  directions.  Rosenbach  lays  stress  on  the  increase  or  movabil- 
ity  of  dulness  to  the  right  when  the  patient  lies  on  his  right  side. 

Although  Bauer  agrees  in  the  statement  that  the  flat  area  of 
pericardial  effusion  may  be  recognised  by  its  characteristic  pear- 
shaped  outline^  he  nevertheless  expresses  the  opinion  that  more 
importance  should  be  attached  to  the  surrounding  zone  of  relative 
dulness,  "  since,  indeed,  the  absolute  cardiac  dulness  not  uncom- 
monly in  cases  of  well-marked  effusion  show^s  little  or  no  altera- 
tion." 

In  cases  of  extreme  pericardial  effusion  the  base  of  this  flat 
area  may  extend  nearly  across  the  anterior  surface  of  the  chest, 
from  within,  or  in  some  cases  even  outside  the  right  mamillary 
line,  to  a  variable  distance  outside  the  left  mamillary  or  to  the  left 
anterior  axillary  line.  In  consequence  of  the  depression  of  the 
left  lobe  of  the  liver  caused  by  the  weight  of  the  distended  sac, 
the  inferior  margin  of  this  area  may  reach  as  low^  as  the  sixth,  or 
in  extreme  cases  even  the  seventh  left  intercostal  space,  while  its 
broad  conical  apex  may  extend  as  high  as  the  level  of  the  second 
costal  cartilage  or  the  first  interspace. 

When  this  flat  area  has  attained  such  proportions  it  is  usually 
not  difficult  to  determine  the  nature  of  the  case.  Yet,  since  a 
greatly  dilated  heart  may  also  crowd  aside  the  lungs  and  occasion 
a  similar  extension  of  the  area  of  cardiac  dulness,  error  can  only 
be  avoided  by  attention  to  the  following  points:  (1)  When  the 
pericardial  sac  is  distended  by  fluid  its  left  latero-inferior  bound- 
ary extends  beyond  the  situation  of  the  apex-beat,  and  hence  this 
latter,  as  determined  by  auscultation,  is  found  situated  within  and 
above  the  extreme  left  lower  angle  of  cardiac  dulness.     In  dilata- 


78 


DISEASES   OF   THE    HEART 


tion  of  the  heart,  on  the  other  hand,  it  is  the  organ  itself  which 
determines  the  dulness,  and  therefore  the  apex-beat  corresponds 
with  the  onter  and  lower  limit  of  cardiac  dulness.  Leube  lays 
great  stress  on  this  point  in  the  differential  diagnosis  of  these  two 
conditions.  (2)  In  cases  of  pericardial  effusion  the  line  of  de- 
marcation between  the  area  of  flatness  and  surrounding  pulmo- 
nary resonance  is  very  abrupt,  while  in  cardiac  dilatation  the 
transition  from  flatness  to  resonance  is  much  less  pronounced. 
Bauer  and  Sansom  both  attach  great  importance  to  the  abruptness 
of  this  transition  in  cases  of  pericardial  effusion.  At  the  same 
time  one  should  not  forget  the  fact  that  occasionally  the  distended 
sac  may  be  overlapped  by  the  lungs,  and  therefore  absolute  dulness 
may  shade  off  through  a  surrounding  zone  of  comparative  dulness 
into  full  pulmonary  resonance. 

When  pericardial  effusion  takes  place  the  first  change  notice- 
able upon  percussion  is  the  development  of  a  small  triangular  area 

of  dulness  in  the  fifth  right  in- 
tercartilaginous  space,  or,  as 
the  Germans  term  it,  in  the 
cardio-hepatic  angle  (Fig.  18). 
This  sign,  first  described  by 
Rotch,  and  sometimes  called 
Botch's  sign,  is  due  to  the  fact 
that  when  eft'usion  collects  it 
first  distends  the  sac  at  its 
lower  right  corner,  occupying 
the  space  between  the  curved 
inferior  margin  of  the  heart 
and  the  upper  line  of  hepatic 
dulness  immediately  to  the 
right  of  the  lower  end  of  the 
sternum.  Ewart  and  Ebstein 
have  also  directed  attention  to 
the  occurrence  of  this  small 
triangular  dull  patch. 

Xormally,  the  outer  bound- 
ary of  cardiac  dulness  over  the  right  auricle  presents  a  curved 
line,  passing  from  the  level  of  the  third  costal  cartilage  downward 
and  outward,  and,  after  crossing  the  fourth  cartilage,  passes  in- 


ili..     i^. i;<r|l  irM    SjliN    (IK    lJK(il.NNlNU 

Pekicaudial  Effusion. 

Dulnesa  in  sliaded  area  or  cardio-hepatic 
an^rle:  c.d.,  cardiac  dulness  ;  h.d.,  hepatic 
dulness. 


PERICARDITIS  WITH  EFFUSION  T9 

ward  as  well  as  downward  to  join  the  inferior  margin  of  the  right 
ventricle.  (See  Fig.  2.)  In  the  formative  stage  of  pericardial 
effusion,  on  the  contrary,  the  right  border  of  heart-dulness  is  no 
longer  curved,  but  passes  directly  downward,  joining  liver-dulness 
at  an  abrupt  angle.  Rotch's  sign  is  therefore  of  great  value  in 
determining  the  beginning  of  pericardial  effusion. 

One  occasionally  sees  statements  to  the  effect  that  an  altera- 
tion in  the  extent  of  cardiac  dulness  depending  upon  the  patient's 
position  makes  strongly  for  pericarditis  with  effusion.  This  is 
nevertheless  a  very  untrustworthy  sign,  since,  if  the  heart  is 
greatly  enlarged,  it  may  fall  away  from  the  anterior  chest-wall  in 
the  dorsal  decubitus  with  consequent  diminution  of  cardiac  dul- 
ness, and  in  the  erect  posture  again  approach  the  anterior  parietes 
and  occasion  a  corresponding  increase  in  the  heart's  area.  ]Sro 
inconsiderable  danger  of  fatal  syncope  sometimes  attaches  to  the 
patient's  change  of  position  from  the  recumbent  to  the  erect,  and 
since  the  sign  just  alluded  to  is  of  but  slight  value,  one  is  hardly 
justified  in  thus  subjecting  a  patient  with  pericarditis  to  the  risk 
of  sudden  death. 

Auscultation. — As  a  rule,  the  pericardial  friction-sound  of  the 
first  stage  disappears  with  the  occurrence  of  effusion,  to  reappear 
after  absorption  has  again  allowed  the  roughened  pericardial  sur- 
faces to  come  in  contact.  ISTevertheless  all  writers  agree  in  stat- 
ing that  the  persistence  of  the  friction-sound  is  not  incompatible 
with  a  considerable  amount  of  fluid,  even  as  much  as  a  quart 
(Cejka),  in  the  pericardial  sac.  The  explanation  of  the  non- 
disappearance  of  the  friction-sound  in  such  cases  is  found  in  the 
presence  of  adhesions  over  the  body  of  the  heart,  which  prevent 
the  separation  of  the  epicardium  from  the  pericardium,  and  force 
the  fluid  to  the  dependent  parts  surrounding,  or  in  failure  of  the 
sac  to  be  completely  filled.  In  other  instances  the  friction-sound 
becomes  faint  when  not  wholly  inaudible. 

Any  alteration  that  takes  jDlace  in  the  heart-sounds  affects  their 
intensity  rather  than  their  quality,  since  they  have  to  be  trans- 
mitted to  the  ear  from  a  distance  proportionate  to  the  recession 
of  the  heart  from  the  chest-wall  and  through  a  layer  of  fluid. 
If  the  effusion  is  massive  and  fills  the  sac  to  its  utmost  capacity 
the  cardiac  tones  may  be  inaudible,  but  this  is  so  rare  that  I  have 
never  observed  a  case  in  which  they  were  wholly  absent.     In  most 


80 


DISEASES   OF   THE   HEART 


cases  the  sounds  at  the  apex  are  feeble,  but  not  wanting,  while  at 
the  base  they  are  heard  more  clearly.  The  pulmonic  second  sound 
is  accentuated  and  the  aortic  sound  is  diminished. 

In  a  recently  observed  case  of  extensive  pericardial  effusion 
in  a  child  the  cardiac  impulse,  the  sounds,  and  a  previously  ex- 
isting endocardial  murmur  all  remained  distinct  over  the  body  of 
the  organ,  and  were  attributed  to  the  presence  of  adhesions  that 
had  forced  the  fluid  to  the  side  of  the  sac. 

Secondary  Physical  Signs  lleferahle  to  the  Lungs. — Valuable 
information  of  the  existence  of  pericardial  effusion  may  also  be 
obtained  by  examination  of  the  lungs.  The  retraction  and  com- 
pression of  pulmonary  tissue  occasions  a  loss  of  normal  pulmonary 
resonance  in  the  neighbourhood  of  the  sac.  In  the  left  infra- 
clavicular region  percussion  elicits  Skodaic  resonance,  or  if  the 
compression  be  very  great,  impairment  of  the  note.   Both  Pins  and 

Ewart  have  called  attention  to 
certain  changes  discoverable 
by  percussion  and  auscultation 
at  the  posterior  base  of  the  left 
lung.  The  "■  Pins'  sign  "  is 
dulness  and  bronchial  breath- 
ing in  the  left  infrascapular 
region,  which,  upon  the  pa- 
tient leaning  forward,  give 
way  to  tympanitic  resonance, 
eiT'pitant  rales,  and  finally 
vesicular  breathing.  This  dul- 
ness and  bronchial  breathing 
can  hai'dly  be  attributed  to 
])louritic  effusion,  if  one  bears 
in  mind  the  curved  upper  line 
of  the  dulness  in  this  latter 
affection. 

Ewart  has  described  a  pos- 
terior ])atcli  of  dulness  in  cases  of  extensive  pericardial  effusion 
situated  at  the  base,  and  which,  extending  from  the  spinal  column 
outward  nearly  or  quite  to  a  line  corresponding  witli  the  internal 
border  of  tlie  scapula,  turns  abru])tly  u))ward  at  a  right  angle,  and, 
after  reaching  the  level  of  the  ninth  or  tenth  dorsal  spine,  again 


Fio.  lit." — 1,'i.  ii'ix  Ki  I'l  i.mmnakv  Changes 
IN  Pins'  (P)  and  Ewart's  (E)  Signs 
OF  Pericakdial  FIffi-sion. 


PERICARDITIS   WITH  EFFUSION  81 

turns  sharply  inward  to  reach  the  side  of  the  vertebral  column 
(Fig,  19).  Over  this  patch  breath-sounds  are  wanting  and  voice- 
sounds  are  feeble.  Occasionally  a  similar  dull  area  may  be 
found  to  the  right  of  the  spine.  Ewart  attributes  this  sign 
to  "  altered  dorsal  relation  of  the  liver."  Immediately  below 
and  to  the  left  of  the  tip  of  the  left  scapula,  especially  in  children 
(Sansom),  is  a  dull  patch  of  about  2  inches  diameter,  in  which  are 
bronchial  breathing  and  bronchophony  or  segophony.  Ewart  has 
also  directed  attention  to  a  somewhat  inconstant  sign  consisting  of 
a  small  area  of  bronchial  breathing  in  the  right  mamillary  line, 
between  the  right  nipple  and  the  upper  surface  of  hepatic  dul- 
ness. 

Diagnosis. — As  a  rule  it  is  not  difficult  to  determine  the  ex- 
istence of  pericardial  exudation  when  this  is  abundant,  but  it  is 
not  easy  nor  always  possible  to  determine  its  nature.  If  the  peri- 
carditis arises  in  the  course  of  articular  rheumatism,  and  signs  of 
distention  of  the  sac  present  themselves,  the  exudation  is  probably 
sero- fibrinous.  Of  324  cases  of  fatal  pericarditis  occurring  at  the 
Berlin  Charite  between  1866  and  1876,  and  which  were  analyzed 
by  Breitung  (Eichhorst),  sero-fibrinous  was  found  108  times,  as 
against  24  of  purulent  and  30  of  hsemorrhagic  exudation.  Fur- 
thermore, the  nature  of  the  primary  affection  to  which  the  peri- 
carditis is  attributable  is  of  diagnostic  significance,  since  it  is 
likely  to  determine  the  nature  of  the  exudate.  If  the  inflamma- 
tion occurs  in  the  course  of  septicaemia,  or  results  from  extension 
of  empyema,  or  from  the  perforation  of  a  gastric  ulcer,  from  a 
perforating  wound,  etc.,  it  is  likely  to  be  purulent.  The  appear- 
ance of  distinct  septic  phenomena,  rigors,  and  an  irregular  inter- 
mittent fever,  profuse  perspirations,  great  and  rapidly  increasing 
prostration,  a  dry,  coated  tongue,  diarrhoea,  etc.,  warrants  the 
diagnosis  of  pyopericardium. 

If  signs  of  fluid  distention  of  the  sac  develop  rapidly  in  the 
course  of  scorbutus  or  purpura  haemorrhagica  or  some  other  dys- 
crasia,  as  cancer,  and  particularly  if  accompanied  by  pronounced 
and  rapidly  increasing  antemia,  the  probability  is  in  favour  of  a 
hsemorrhagic  pericarditis.  Inasmuch,  however,  as  such  theoretical 
distinctions  in  the  sjnnptomatology  of  the  three  varieties  are  not 
always  clearly  defined,  a  differential  diagnosis  is  often  only  possi- 
ble by  means  of  exploratory  puncture. 


82  DISEASES  OF   THE   HEART 

Differential  Diagnosis. — Before  considering  the  differentia- 
tion of  fluid-collection  within  the  pericardium  from  certain  other 
conditions  with  which  it  may  be  confounded,  it  is  well  to  speak 
of  the  ditiiculty  of  diagnosis  arising  from  pulmonary  emphysema 
and  old  adhesions  that  date  from  a  previous  attack  of  pericarditis. 
Emphysema  may  prevent  the  lung-margins  from  being  crowded 
aside,  and  hence  the  characteristic  area  of  cardiac  flatness  may 
not  exist.  In  such  an  event  reliance  must  be  placed  on  the  outline 
of  deep-seated  dulness,  and  this  failing,  absolute  diagnosis  is 
hardly  possible.  When  old  adhesions  exist  over  the  front  of  the 
heart  they  force  the  exudate  to  accumulate  at  the'  sides  and  bot- 
tom of  the  sac  or  to  be  pent  up  posteriorly.  Accumulation  of  fluid 
along  the  lateral  and  inferior  margins  causes  increase  of  dulness 
in  these  situations,  its  triangular  outline  being  fairly  well  main- 
tained. In  addition,  the  cardiac  impulse  and  tones,  together  with 
the  friction-rub,  remain  botli  palpable  and  audible  over  the  body 
of  the  organ. 

When  effusion  is  confined  to  the  posterior  aspect  of  the  sac  its 
recognition  is  most  difficult,  if  not  impossible.  In  such  a  case  one 
must  rely  mainly  on  the  symptoms  of  (1)  inflammation,  as  pain 
and  fever,  and  (2)  of  a  deeply  situated  collection  of  fluid  and 
pressure  on  the  (Psophagus  and  bronchi,  dysphagia,  and  dyspmra. 
The  last  two  symptoms  are  very  suggestive  of  exudation  into  the 
posterior  portion  of  the  sac.  Massip  calls  this  an  Encysted  Peri- 
carditis with  retrocardiac  effusion,  and  says  its  symptoms  are  so 
obscure  that  one  can  do  no  more  than  diagnose  the  pericarditis 
without  being  able  to  decide  whether  effusion  is  present  or  not. 
He  thinks  that  dulness  at  the  left  posterior  base  with  muffling  or 
absence  of  heart-tones  in  this  region,  together  with  signs  of  pres- 
sure on  the  oesophagus  and  of  active  pericardial  inflammation,  are 
strongly  suggestive  of  a  posterior  effusion. 

Dilatation  of  the  heart  is  the  condition  which  most  often  has 
to  bo  differentiated  from  pericardial  effusion.  The  enlargement 
of  the  organ  causes  retraction  of  the  lung-borders  and  an  area  of 
dulness  very  like  that  of  effusion,  and  if  the  heart-tones  and  im- 
pulse are  very  feeble,  from  fatty  degeneration,  a  precise  diagnosis 
may  under  certain  circumstances  be  extremely  difficult.  The  main 
point  on  which  reliance  is  placed  is  not,  as  sometimes  stated, 
greater  distinctness  of  heart-shock  and  sounds   in  dilatation   as 


PERICARDITIS   WITH  EFFUSION  83 

compared  with  effusion,  but  is  the  position  of  the  apex-beat  with 
relation  to  the  outer  and  inferior  margin  of  dulness  (see  page 
77).  Theoretically  this  is  very  fine,  but  every  experienced  clini- 
cian knows  that  in  many  cases  it  is  impossible  to  say  definitely 
whether  they  correspond  or  not  on  account  of  the  indistinctness 
and  diffuseness  of  the  cardiac  impulse.  I  once  saw  the  late  dis- 
tinguished von  Ziemssen,  one  of  Germany's  most  skilful  clinical 
teachers,  make  a  mistake  in  just  such  a  case.  The  patient,  who 
was  in  extremis,  was  presented  to  the  class  as  an  instance  of 
massive  pericardial  exudation.  There  was  a  large  triangular  area 
of  absolute  cardiac  dulness  over  which  impulse  was  wanting,  and 
heart-sounds  were  scarcely  audible.  Moreover,  rtdes  of  acute  pul- 
monary oedema  rendered  auscultation  highly  unsatisfactory.  The 
autopsy,  next  day,  disclosed  a  fatty  and  extremely  dilated  heart, 
but  no  effusion,  and  von  Ziemssen  took  the  occasion  to  teach  a 
most  instructive  lesson  on  the  difiiculties  of  differential  diagnosis. 

Should  it  jDrove  impossible  to  locate  the  apex-impulse  in  the 
recumbent  posture,  the  patient  may  be  slowly  and  cautiously  lifted 
into  the  erect  position  in  the  hope  of  the  heart  gravitating  for- 
ward, and  thus  declaring  the  situation  of  its  apex.  If  this  not 
entirely  safe  procedure  fails,  then  aid  may  sometimes  be  derived 
from  careful  study  of  the  pulse,  which  in  pericardial  effusion  is 
said  to  occasionally  be  relatively  stronger  than  the  feebleness  of 
the  heart-sounds  would  lead  one  to  expect. 

This  is  also  a  theoretical  point  which  I  have  never  found  to 
stand  the  test  of  practical  experience.  When  a  pericardial  exu- 
dation is  massive,  as  well  as  when  extreme  dilatation  sinaulates 
effusion,  the  equilibrium  of  circulation  is  lost,  the  veins  are  over- 
filled, and  the  arterial  system  is  empty,  so  that,  as  a  matter  of  fact, 
the  pulse  of  extensive  effusion  is  small,  weak,  and  rapid.  Should 
all  attempts  to  arrive  at  a  differential  diagnosis  fail,  then,  as  sug- 
gested by  Leube,  we  may  have  recourse  to  digitalis  and  other 
therapeutic  measures  in  the  hope  of  clearing  up  the  condition. 
In  dilatation  proper  treatment  may  revive  the  flagging  heart  and 
restore  the  apex-beat  and  heart-sounds,  while  in  pericarditis  it  may 
cause  absorption  of  fluid  and  a  reappearance  of  pericardial 
friction. 

Pleurisy  with  effusion  may  be  mistaken  for  pericarditis,  or 
rather  a  pericardial  may  be  considered  a  pleuritic  effusion.     There 


84  DISEASES   OF  THE  HEART 

is  much  similarity  in  the  pain,  fever,  and  dyspnoea,  as  well  as  cer- 
tain pressure-effects,  but  error  is  avoidable  by  attention  to  the  fol- 
lowing points:  (1)  In  pleuritic  effusion  there  is  a  curved  line  of 
flatness  which  extends  from  the  back  around  the  side  to  the  front, 
which  line  usually  shifts  with  change  in  the  patient's  position. 
(2)  A  left-side  effusion  (the  only  one  likely  to  lead  to  error) 
pushes  the  heart  over  to  the  right  of  the  median  line.  (3)  Breath- 
sounds  at  the  left  base  are  diminished  or  absent,  instead  of  exag- 
gerated or  bronchial,  as  in  pericardial  effusion.  (4)  Dysphagia 
is  very  rarely  if  ever  present  in  pleurisy.  (5)  In  pericarditis 
there  is  usually  a  history  of  rheumatism  or  other'  acute  infectious 
process  to  lead  to  cardiac  involvement.  In  an  adult  a  differential 
diagnosis  between  these  two  affections  is  seldom  difficult,  but  I 
have  seen  young  children  in  whom  it  was  at  first  not  at  all  easy  to 
say  which  was  the  process,  owing  to  the  great  compression  of  the 
left  lung  and  consequent  extent  of  dulness  laterally  and  behind. 

The  foregoing  are  the  only  two  affections  likely  to  mislead ; 
yet  the  careless,  and  still  more  the  inexperienced,  may  mistake 
for  pericarditis  a  number  of  conditions  that  occasion  increase  in 
cardiac  dulness  upward  and  to  the  left.  These  are  mediastinal 
tumours,  which  crowd  the  lung-margins  aside  and  displace  the 
heart,  and  pulmonary  tuberculosis  or  old  pleuritic  adhesions, 
which  cause  permanent  retraction  and  fixation  of  the  anterior  bor- 
der of  the  left  lung.  Error  ought  to  be  avoided,  however,  by  due 
attention  to  history,  symptoms,  and  physical  findings.  The  history 
is  that  of  insidious  commencement  and  slow  course — symptoms 
are  those  of  a  chronic  process  without  fever,  except,  of  course,  in 
the  case  of  pulmonary  tuberculosis,  when  there  is  characteristic 
sputum  to  act  as  a  guide — and  as  regards  clinical  findings,  the 
dulness  lacks  the  distinctively  triangular  shape  of  pericarditis 
with  effusion.     Time  settles  the  diagnosis  beyond  question. 

Prognosis. — This  depends  upon  the  nature  of  the  exudate, 
the  rapidity  of  its  formation,  its  amount,  the  effect,  both  of  in- 
flammation and  resulting  effusioii  upon  the  myocardium,  the  ex- 
istence of  complications,  as  acute  or  chronic  endocarditis,  Bright's 
disease,  tuberculosis,  etc.,  and  finally,  the  age  and  vitality  of  the 
patient. 

Suppurative  pericarditis,  unless  recognised  and  treated  surgi- 
cally, is  very  likely  to  prove  fatal,  and  yet,  as  previously  stated, 


PERICARDITIS  WITH  EFFUSION  85 

if  of  rather  a  benign  type  the  fluid  portion  of  the  exudate  may 
ultimately  become  absorbed,  leaving  a  cheesy,  and  at  times  a  cal- 
careous, mass  behind. 

Pericarditis  hcemorrliagica  acuta  may  destroy  life  within  a 
few  days.  When  the  malady  is  chronic,  its  prognosis  is  essentially 
that  of  the  scorbutus  or  other  primary  affection. 

An  effusion  of  whatever  nature  that  forms  rapidly  and  to  a 
large  amount  is  always  serious,  because  time  is  not  allowed  for  the 
system  to  adjust  itself  to  the  altered  conditions.  Such  a  case  may 
speedily  prove  fatal.  If  the  inflammation  extends  to  the  myo- 
cardium, or  if  this  latter  has  undergone  previous  degeneration, 
the  heart-muscle  will  be  ill  prepared  to  sustain  the  pressure  ex- 
erted by  the  fluid  confined  within  the  tense  and  resisting  sac. 
Serious  circulatory  and  respiratory  embarrassment,  or  the  possibil- 
ity of  fatal  syncof)e,  renders  the  immediate  prognosis  most  grave. 

Acute  endocarditis  is  a  serious  complication,  and  the  existence 
of  a  chronic  valvular  lesion  occasions  a  degree  of  gravity  which 
might  not  be  the  case  if  the  pericarditis  existed  alone.  If  the  dis- 
ease occurs  in  a  person  with  acute  or  chronic  nephritis,  or  if  pul- 
monary tuberculosis  coexists,  the  patient  is  hardly  in  condition  to 
successfully  cope  with  the  occurrence  and  long  duration  of  an  exu- 
dative pericarditis.  Moreover,  coming  on  as  it  does  toward  the 
end  of  chronic  nephritis,  the  pericarditis  contributes  largely  to  the 
fatal  result. 

Finally,  emphasis  has  been  repeatedly  laid  on  the  serious  na- 
ture of  pericarditis  in  children,  owing  to  the  frequency  with  which 
it  implicates  the  heart-muscle  and  the  strong  likelihood  of  its 
leading  to  cardiac  dilatation.  In  children,  therefore,  the  imme- 
diate, as  well  as  the  ultimate  prognosis,  is  serious.  In  old  people 
and  those  enfeebled  by  some  chronic  malady  that  has  brought  them 
to  a  state  of  cachexia  there  is  small  likelihood  of  the  patient  sur- 
viving until  time  can  bring  about  absorption  of  the  effusion. 

In  all  cases,  even  when  death  does  not  result  directly  from  the 
acute  inflammatory  or  exudative  process,  there  is  a  possibility  of 
the  heart  being  crippled  by  inflammatory  damage  to  the  myocar- 
dium, or  by  partial  or  total  obliteration  of  the  sac.  Of  the  324 
cases  analyzed  by  Breitung,  there  were  circumscribed  adhesions  in 
111,  and  complete  adhesion  of  the  pericardium  in  23.  The  remote 
prognosis  depends  upon  the  richness  of  the  exudate  in  fibrin;  in 


86  DISEASES   OF   THE   HEART 

such  the  likelihood  of  adhesions  is  the  greater.  Pericardial  in- 
flammation, therefore,  of  whatever  nature,  should  never  be  looked 
upon  as  a  trivial  complaint. 

Treatment. — We  possess  no  means  of  arresting  an  attack  of 
pericarditis,  and  therefore  we  must  content  ourselves  with  en- 
deavouring to  combat  the  rheumatism  or  other  affection  in  the 
course  of  which  pericardial  inflammation  occurs,  in  the  hope  of 
preventing  the  latter.  If,  nevertheless,  the  sac  becomes  involved, 
we  must  strive  to  lessen  the  severity  of  the  process,  and  this  fail- 
ing, to  relieve  symptoms  and  sustain  the  powers  of  life  until  the 
disease  comes  to  a  natural  termination. 

Inasmuch  as  we  are  powerless  to  abruptly  terminate  pericar- 
ditis, and  it  occurs  most  often  in  the  course  of  articular  rheuma- 
tism, every  possible  effort  should  be  made  to  cut  short  or  mitigate 
the  intensity  of  the  rheumatic  attack.  This  is  no  place  to  discuss 
the  treatment  of  the  latter  affection,  yet  I  wish  to  record  my  con- 
fidence in  the  salicylic-acid  treatment,  especially  in  methylsalicyl- 
ate,  both  locally  and  internally.  If  this  is  not  a  specific,  we  at  all 
events  possess  nothing  better,  and  must  await  the  time  when  defi- 
nite knowledge  of  its  nature  may  supply  us  with  an  efficient 
weapon  against  rheumatism. 

The  importance  of  physical  rest  cannot  be  too  strongly  in- 
sisted upon  whenever  fever  or  other  rheumatic  symptoms  make 
their  appearance.  This  is  particularly  wise  in  the  case  of  children 
who  have  an  old-standing  valvular  lesion.  Such  children  ought  to 
be  seen  by  the  family  doctor  whenever  sore  throat  or  other  sus- 
picious symptoms  arise.  Physical  exertion  by  increasing  the  force 
and  frequency  of  cardiac  contractions,  tends  not  only  to  intensify 
pericarditis  wdien  it  is  already  present,  but  may  even  determine 
its  development  in  the  same  way  that  use  of  a  rheumatic  joint 
may  aggravate  the  arthritis.  If  an  adult  is  unwilling  to  submit 
to  rest,  he  should  be  informed  of  the  possibility  of  endocardial  or 
pericardial  inflammation,  and  thus  perhaps  be  induced  to  take 
proper  care  of  himself. 

When  pericarditis  once  sets  in,  measures  are  indicated  to  lessen 
its  intensity.  Vesication  of  the  pra'cordia  was  once  extensively 
used  for  this  purpose,  and  there  arc  still  many  physicians  who 
believe  in  the  efficacy  of  this  treatment  in  the  initial  stage.  Per- 
sonally, I  am  sceptical  of  tlic  influence  of  blisters  in  this  regard, 


PERICARDITIS  WITH   EFFUSION  87 

and  believe  that  milder  measures  will  do  just  as  much  good,  while 
at  the  same  time  saving  the  patient  from  the  pain  and  discomfort 
of  a  large  blister.  The  real  benefit  of  vesication,  in  my  opinion, 
is  found  in  the  relief  of  pain,  and  therefore  I  think  it  is  prefer- 
able to  adopt  small  blisters,  a  fresh  one  being  applied  so  soon  as 
the  previous  one  has  filled.  This  is  the  plan  advocated  by  Caton, 
because  of  the  ease  to  pain  thus  afforded.  I  have  had  no  great 
experience  with  this  mode  of  treatment,  because  I  prefer  the 
application  of  cold  to  the  cardiac  area.  I  know  that  counter- 
irritation  often  eases  the  suffering  occasioned  by  inflammation 
of  serous  membranes,  and  therefore  advise  that  if  cold  is  not  well 
borne  and  the  intensity  of  the  initial  pain  seems  to  call  for  some 
measure  of  the  kind,  that  this  be  a  sinapism  made  of  English  mus- 
tard by  the  nurse,  and  that  it  be  left  on  until  the  skin  becomes 
thoroughly  reddened.  When  the  mustard-draught  is  removed,  its 
place  may  be  supplied  by  a  poultice  or  by  hot  fomentations.  Moist 
heat  to  the  prsecordium  gives  great  relief  in  some  cases,  and  is 
much  extolled.  Roberts  applies  2  or  3  leeches  over  the  heart  in 
suitable  cases,  but  as  a  rule  finds  poulticing  in  the  early  stage  gives 
positive  relief  to  pain. 

Lees  is  a  strong  advocate  of  the  continuous  use  of  the  ice-hag, 
and  asserts  that  it  not  only  gives  comfort  by  alleviating  pain  and 
palpitation,  but  tends  to  mitigate  the  severity  of  the  inflammatory 
process.  This  mode  of  treatment  has  always  appealed  to  me  as 
rational,  and  in  all  cases  in  which  I  have  seen  its  use  faithfully 
tried  it  has  appeared  to  be  very  comforting  and  agreeable.  The  ice- 
bag  must  be  light,  so  as  not  to  oppress  the  patient  by  its  weight, 
and  should  be  held  in  place  by  a  cord  passing  around  the  neck. 
As  the  sufferer  is  usually  in  a  semi-recumbent  posture,  the  bag, 
thus  suspended,  rests  lightly  on  the  praecordia  without  danger  of 
slipping  off.  Furthermore,  the  ice-bag  must  not  be  allowed  to  rest 
against  the  bare  skin,  as  it  is  apt  to  occasion  irritation,  but  a  small 
piece  of  dry,  thin  cloth  is  to  be  interposed  between  the  surface  of 
the  chest  and  the  bag.  In  this  manner  the  bag  is  generally  well 
borne,  when  before  it  could  not  be  endured.  Children  are  some- 
times uneasy  at  first,  yet  if  the  application  of  cold  is  firmly  in- 
sisted upon,  they  not  only  learn  to  tolerate  it,  but  actually  find 
it  soothing.  Should  idiosyncrasy  render  an  individual  absolutely 
intolerant  of  cold,  then  it  may  be  replaced  by  poultices.     Hot  fo- 


88  DISEASES  OF   THE   HEART 

mentations  are  objectionable  on  account  of  the  liability  of  their 
wetting  the  clothing,  and  of  a  chill  when  the  cloths  are  changed. 
In  the'  employment  of  the  poultice  due  attention  should  be  paid  to 
the  principle  that  to  be  efficacious  it  must  be  hot,  not  merely  warm, 
and  must  be  replaced  by  a  fresh  one  so  soon  as  it  grows  cool. 
When  at  length  poultices  are  discontinued  the  surface  of  the  chest 
must  be  covered  by  a  layer  of  cotton  or  flannel. 

Treatment  in  the  inflammatory  stage  is  largely  symptomatic, 
and  in  most  cases  something  more  than  either  heat  or  cold  is  re- 
quired to  allay  pain  and  restlessness.  In  mild  cases  an  anodyne 
liniment,  as  belladonna,  chloroform,  or  one  containing  morphine, 
may  suffice,  and  should  be  tried  before  recourse  is  had  to  internal 
medication. 

When  pain  and  restlessness  are  severe  nothing  is  so  serviceable 
as  opium  in  some  form.  In  the  case  of  adults  a  hypodermic  of 
morjDliine  is  the  best ;  to  children  it  is  far  better  to  give  the  remedy 
by  the  mouth.  Their  well-known  susceptibility  to  the  drug  makes 
it  advisable  to  try  the  effect  of  codeine  before  resorting  to  opium 
or  morphine.  In  some  cases  it  will  be  found  that  a  combination 
of  codeine  and  sodium  bromide  ^^'ill  act  efficiently  and  render 
more  powerful  remedies  unnecessary — a  consideration  to  be  al- 
ways borne  in  mind  with  children. 

Besides  allaying  pain  and  quieting  the  little  sufferers,  these 
agents  tend  to  lessen  the  violence  of  heart-action — a  desideratum  of 
importance — and  to  promote  sleep.  Insomnia  is  often  very  trou- 
blesome, and  when  not  overcome  it  contributes  greatly  to  the  pa- 
tient's nervousness  and  inability  to  bear  well  the  strain  of  a  pro- 
tracted illness,  which,  like  pericarditis,  makes  great  demands  on 
the  patient's  powers  of  endurance.  An  opiate  steadies  the  nerves, 
and  if  it  does  not  too  greatly  disturb  digestion  and  secretion  I 
believe  it  cruel  to  withhold  it  in  cases  characterized  by  the  fore- 
going symptoms. 

Cough  is  an  annoying  feature  in  some  cases,  and  when  this 
is  so  it  affords  an  additional  reason  for  the  administration  of 
codeine  or  morj)hino.  A  preferable  remedy,  however,  is  heroin, 
wliich  to  an  adult  may  be  given  in  the  dose  of  -^  grain,  and  to 
children  in  proportionately  smaller  amounts.  It  not  only  allays 
cough  efficiently,  but  is  devoid  of  the  inipleasant  after-effects  of 
morphine. 


PERICARDITIS    WITH  EFFUSION  89 

Nausea  and  vomiting  may  in  some  cases  tax  medical  skill  to 
the  utmost,  and,  as  in  a  recently  observed  instance,  defy  all  at- 
tempts to  allay  them.  In  such  an  event  it  becomes  necessary  to 
stop  oral  administration  of  food  and  medicines,  and  to  rely  on 
enemata  in  the  hope  of  the  stomach  becoming  quiet. 

Fever  does  not  always  require  antipyretic  treatment,  but  should 
it  persist  at  102°  F.  or  higher  it  may  be  reduced  by  sponging. 

In  this  early  stage  rapid,  violent  action  of  the  heart  is  often 
present,  and  seems  to  call  for  quieting  measures.  Digitalis  does 
not  appear  to  me  to  be  indicated,  for  tachycardia  is  now  not  a 
manifestation  of  weakness,  but  of  irritation,  and  in  my  experi- 
ence the  heart  does  not  bear  kindly  attempts  to  slow  it  by  digitalis. 
Neither  should  aconite  or  veratrum  be  prescribed  for  this  purpose, 
since  they  are  too  depressing,  and  the  heart  is  likely  to  need  all  its 
reserve  force  before  the  struggle  is  over.  I  believe  no  therapeu- 
tic measure  is  more  efficient  in  quieting  the  organ  than  an  ice-bag 
worn  continuously. 

The  routine  administration  of  digitalis  is  objectionable  in  any 
form  of  cardiac  disease,  and  in  pericarditis  is  especially  so.  The 
real  indication  for  its  use  in  this  affection  is  not  merely  rapidity 
of  the  pulse,  but  feebleness,  together  with  rapidity.  Therefore, 
should  the  unchecked  tachycardia  begin  at  length  to  tell  on  the 
heart,  or  should  the  organ  furnish  signs  of  dangerous  dilatation 
with  scantiness  of  urine  and  other  evidences  of  visceral  conges- 
tion, then  it  is  well  to  prescribe  digitalis.  The  hypodermic  ad- 
ministration of  digitalin  does  not  seem  to  me  so  reliable  or  effec- 
tive as  the  internal  use  of  a  fat-free  tincture,  or  of  the  infusion 
in  moderate  doses,  10  drops  of  the  former  and  a  tablespoonful  of 
the  latter  to  an  adult,  and  to  a  child  a  proportionately  smaller 
amount  every  four  to  six  hours. 

Strychnine  is  a  heart-tonic  which  cannot  be  dispensed  with  in 
this  stage.  Its  dose  does  not  need  to  be  large  at  first,  perhaps  -gV 
if  the  patient  is  grown,  3  or  4  times  a  day.  It  may  be  given  by 
the  mouth,  but  under  the  skin  is  preferable,  since  its  action  is 
more  direct  and  powerful. 

There  is  always  a  more  or  less  pronounced  tendency  to  con- 
gestion in  pericarditis,  the  liver  feeling  the  brunt  of  the  attack, 
and  hence  being  usually  palpable.  Consequently  it  is  well  to  re- 
lieve visceral  and  portal  congestion  by  a  mild  daily  laxative,  calo- 


90  ■  DISEASES  OF  THE  HEART 

niel  or  a  saline  aperient  water.  Vigorous  depleting  measures  in 
the  inflammatory  stage  are  harmful,  however,  rather  than  bene- 
ficial, and  should  be  reserved  against  the  time  when  fluid  accumu- 
lation occasions  distress. 

Food  must  be  light  and  nutritious,  consisting  largely  of  milk 
and  nourishing  soups  and  broths,  into  which  a  raw  egg  has  been 
dropped.  If  fever  is  not  high,  and  the  patient's  condition  de- 
mands heartier  food,  this  may  be  given  in  the  form  of  chicken, 
raw  oysters,  a  bird,  or  a  small  piece  of  carefully  broiled  beefsteak,, 
with  toast  or  light  biscuit.  An  occasional  eggnog  is  also  excellent. 
It  is  better  to  feed  these  patients  often  and  in  small  amounts  than 
to  supply  them  with  a  hearty  meal  only  3  times  a  day.  Pure 
or  slightly  acidulated  water  should  be  given  freely  so  long  as 
fever  and  thirst  are  present.  It  also  promotes  excretion  and  pro- 
tects the  kidneys  from  the  injurious  effects  of  toxins.  In  most 
cases  skilful  nursing  is  far  more  necessary  and  beneficial  than 
medication. 

Treatment  in  the  Stage  of  Effusion. — With  the  appearance  of 
exudation  and  abatement  of  active  inflammation,  symptoms  of 
pressure  supervene  and  demand  attention.  The  object  of  man- 
agement is  now  threefold:  (1)  to  restrict  the  rapidity  and  amount 
of  effusion,  (2)  to  aid  the  heart  in  its  attempt  to  maintain  circula- 
tion, (3)  to  promote  removal  of  the  exudate  by  absorption  or  other- 
wise. 

In  my  opinion,  it  is  very  doubtful  if  we  possess  any  means  of 
limiting  the  amount  of  effusion,  since  we  have  no  criterion  by 
which  to  estimate  the  efficiency  of  measures  employed  in  any  given 
case.  A  single  large  blister  or  a  succession  of  smaller  ones  over 
the  prai'cordia  is  recommended  by  some  authors ;  but  what  assur- 
ance have  we  that  the  withdrawal  of  serum  in  anywise  diminishes 
the  amount  poured  out  in  the  sac  ?  As  a  matter  of  fact,  the  quan- 
tity of  the  exudate,  and  the  rapidity  of  its  formation,  are  deter- 
mined by  the  intensity  of  the  inflammation.  If,  therefore,  we  are 
to  lessen  the  amount  of  effusion,  we  must  restrain  the  activity  of 
the  inflammatory  process.  Measures  to  this  end  have  already  been 
discussed,  and  although  undoul>tedly  they  should  be  employed, 
their  utility  is  open  to  doubt.  I  pass,  therefore,  to  the  considera- 
tion of  the  second  object  of  treatment. 

In  some  cases  effusion  takes  place  with  such  rapidity  and  in- 


PERICARDITIS  WITH  EFFUSION  91 

duces  such  urgent  pressure-symptoms  that  surgical  interference 
has  to  be  resorted  to  without  delay.  More  often,  however,  indi- 
cations of  pressure  appear  slowly,  and  time  is  afforded  for  a  trial 
of  medicinal  treatment. 

Absolute  rest  is  now  imperative,  and  the  patient,  if  old  enough, 
must  be  advised  of  the  necessity  of  refraining  from  any  sudden 
movement,  lest  it  occasion  fatal  syncope.  He  should  be  supported 
in  a  semi-recumbent  posture  by  a  bed-rest  or  pillows,  and  he  must 
not  be  allowed  to  sit  up  to  take  nourishment  or  medicine.  He 
should  be  disturbed  as  little  as  possible  for  the  purpose  of  examin- 
ing the  heart. 

The  state  of  the  circulation,  as  shown  by  pulse  and  venous 
engorgement,  is  to  be  carefully  watched,  and  so  long  as  the  quality 
and  rate  of  the  pulse  remain  good,  strychnine  may  be  the  only 
heart-tonic  required.  So  soon,  however,  as  the  pulse  shows  dicro- 
tism  or  irregularity  in  force,  size,  and  frequency,  tincture  of  fat- 
free  digitalis  must  be  ordered  in  doses  suitable  to  the  age  of  the 
patient — to  an  adult  10  drops  every  four  to  six  hours. 

The  daily  quantity  of  urine  should  be  accurately  noted,  and  in 
these  cases  a  pronounced  falling  off  of  its  amount  is  an  indication 
for  digitalis,  even  though  the  pulse  remains  fairly  good. 

Careful  examination  of  the  liver  will  always  detect  more  or 
less  engorgement  of  this  organ.  Palpation  of  the  liver  is  often 
painful  or  unsatisfactory  by  reason  of  abdominal  distention,  but 
we  know  by  experience  and  deduction  that  stasis  within  the  por- 
tal system  is  taking  place,  and  hence  hydragogue  cathartics  form 
an  important,  nay  an  indispensable,  part  of  our  therapeutic  meas- 
ures in  this  stage.  By  depleting  the  portal  system  catharsis  aids 
in  maintaining  the  venous  circulation.  Instead  of  weakening  the 
patient,  it  adds  materially  to  his  comfort  by  lessening  epigastric 
pain  and  relieving  abdominal  pressure. 

Sleep  should  be  induced  by  a  hypnotic,  for  nothing  will  more 
surely  tend  to  exhaust  the  nervous  system  than  insomnia.  I  have 
sometimes  foimd  that  the  addition  of  a  :^  or  ^  grain  of  codeine  to 
a  sulphonal  powder  insures  the  action  of  the  latter.  At  this  stage 
morphine  or  a  preparation  of  opium  is  to  be  given  with  very  great 
caution.  It  may  be  indicated  by  dyspnoea  or  restlessness,  but 
actual  danger  attends  the  administration  of  the  drug,  through  its 
depression  of  the  respiratory  centres.     If  it  be  given  to  allay  the 


92  DISEASES  OF   THE   HEART 

dyspnoea,  atropia  should  always  be  added  to  the  morphine,  because 
of  its  well-known  effect  in  deepening  respiration. 

The  passive  congestion  within  the  abdominal  cavity  impairs 
digestion  and  lessens  absorption,  yet  nourishment  is  imperatively 
demanded,  both  by  the  nerve-centres  and  heart-muscle.  Only  such 
food  should  be  given  as  can  be  easily  assimilated,  and  as  but  a 
small  amount  should  be  taken  at  a  time,  it  should  be  concentrated 
and  highly  nutritious.  Some  of  the  prepared  foods  will  now  be 
found  to  be  of  great  service. 

When  by  the  subsidence  of  the  pyrexia,  if  that  has  existed,  it 
is  judged  that  the  active  inflammatory  process  has  ceased,  or  when 
repeated  examinations  of  the  heart  indicate  that  the  amount  of 
effusion  is  stationary,  the  query  naturally  arises.  What  means  are 
to  be  employed  for  its  removal  \  Shall  an  attempt  be  made  to 
promote  this  by  absorption,  or  shall  paracentesis  pericardii  be  per- 
formed? This  brings  up  the  question,  is  absorption  of  the  effu- 
sion possible  ?  Clinical  experience  certainly  gives  an  affirmative 
answer.  Theoretically,  absorption  of  the  exudation  may  be  hin- 
dered or  prevented  by  an  abundant  coating  of  fibrin  over  the 
surface  of  the  pericardium  whereby  the  fluid  cannot  reach  the 
Ijmiphatic  spaces,  or  in  consequence  of  great  venous  stasis  the 
lym])hatic  vessels  may  be  surcharged,  and  the  flow  in  them  be 
too  sluggish  to  promote  active  absorption.  Xevertheless,  particu- 
larly in  rheumatic  cases,  experience  affords  abundant  proof  of 
the  frequent,  even  rapid,  absorption  of  extensive  jiericardial 
effusion. 

Therefore,  I  believe  the  physician  is  culpable  who  refuses  to 
make  the  atteni])t  at  least  to  carry  off  the  fluid  ])y  a  resort  to 
diuretic  and  cathartic  remedies.  xV  great  degree  of  venous  stasis 
often  neutralizes  the  effect  of  diuretics  until  congestion  within  the 
renal  veins  has  been  relieved  by  resort  to  hydragogue  cathartics. 
The  two  classes  of  remedies  should  be  conjoined  therefore.  In  my 
opinion,  the  infusion  of  digiiaJifi  affords  the  best  means  of  estab- 
lishing free  diuresis.  A  tal)les]K)onful  to  begin  with  may  be  ad- 
ministered to  ail  ailult  every  four  iioiiis.  wliilo  tlie  patient  also 
receives  daily  some  unirritating  cathartic,  ca])able  of  inducing  a 
number  of  copious  watery  stools.  I  have  seen  truly  astonishing 
results  follow  such  a  plan  of  treatment.  This  is  well  illustrated 
by  the  case  of  a  boy  of  seven  years  with  mitral  regurgitation  of 


PERICARDITIS  WITH   EFFUSION 


93 


rheumatic  origin,  in  a  state  of  perfect  compensation,  who  had  been 
under  occasional  observation  for  a  year. 

On  May  9,  1899,  he  developed  what  appeared  to  be  a  mild  case 
of  follicular  tonsillitis,  for  which  he  received  appropriate  treat- 
ment. Three  days  later  he  Avas  reported  not  so  v^^ell,  and  at  my 
visit  that  same  day  he  was  found  to  have  a  temperature  of  101°  F. 
He  comjDlained  of  vague  pains  in  the  knees,  which  were  not  red- 
dened or  swollen,  but  showed  an  erythema.  As  the  attack  was  un- 
doubtedly rheumatic,  salicylate  of  soda  was  ordered,  and  as  the  boy 
lived  in  a  suburb  he  was  put  in  charge  of  a  local  physician.  May 
28th  I  was  asked  to  see  him  again,  when  a  prsecordial  fremitus, 
which  disappeared  upon  pressure,  and  a  soft  to-and-fro  murmur, 
quite  different  from  his  endocardial  one,  with  which  I  was  so 
familiar,  left  no  doubt  of  the  existence  of  an  acute  pericarditis. 
The  attending  ph^^sician  stated  that  these  friction-murmurs  had 
developed  a  few  days  previ- 
ously. By  June  5th  the  actual 
increase  in  the  area  of  cardiac 
dulness  gave  evidence  of  the 
occurrence  of  effusion,  though 
the  cardiac  impulse  and  fric- 
tion-sounds still  persisted  over 
the  body  of  the  organ.  Py- 
rexia was  moderate,  pulse  120, 
of  good  quality,  and  respira- 
tions were  accelerated.  An 
ice-bag  had  been  worn  most 
of  the  time  since  May  28th, 
although  pain  had  at  no  time 
been  a  very  marked  feature. 
From  now  on  the  exudation 
increased  steadily  in  amount 
until,  by  June  28th,  the  ex- 
treme limits  of  cardiac  dulness  reached  from  just  within  the 
right  nipple,  quite  to  the  left  axillary  line,  far  outside  the  easily 
located  apex-beat  (see  Fig.  20). 

The  persistence  of  the  pericardial  rub,  somewhat  less  intense, 
to  be  sure,  together  with  palpable  cardiac  impulse  over  the  body 
of  the  heart,  and  the  distinctness  of  the  heart-sounds  and  of  the 


Fig.  20. — Apex-beat  and  Akea  of  Cardiac 
Dulness  in  Case  of  Pericarditis  with 
Effusion. 


94 


DISEASES  OF   THE    HEART 


mitral  regurgitant  inuriiuir,  were  thought  to  indicate  the  existence 
of  adhesions  on  the  anterior  surface  of  the  organ  and  to  have 
prevented  the  eifused  fluid  from  covering  over  the  heart.  That 
the  effusion  was  considerable  was  evinced  by  the  great  distention 
of  the  sac  laterally  and  downward,  by  great  pressure  upon  the 
lungs,  and  pronounced  circulatory  embarrassment.  There  were 
marked  cyanosis,  distention  of  the  superficial  veins,  great  enlarge- 
ment and  tenderness  of  the  liver,  and  slight  ankle  oedema.  Respi- 
rations were  48,  pulse  146,  small,  and  dicrotic,  but  still  regular. 
Salicylate  of  soda  had  been  discontinued  upon  appearance  of  the 
effusion,  lest  it  might  too  greatly  depress  the  heart,  and  as  the 
scanty  urine  was  highly  acid,  bicarbonate  of  soda  and  citrate  of 
potash  had  been  substituted.  As  digitalis  and  mild  cathartics  had 
failed  to  appreciably  diminish  the  amount  of  effusion,  surgical 
interference  was  decided  upon. 

The  selection  of  the  site  of  puncture  was  left  to  me,  and,  be- 
lieving that  in  consequence  of  adhesions  over  the  front  of  the 
heart  the  exudation  could  be  most  surely  reached  at  some  lateral 

point,  I  selected  the  fifth  left 
interspace,  between  the  apex- 
impulse  and  the  outer  margin 
of  flatness  (Fig.  21).  Accord- 
ingly the  surgeon  introduced 
his  trocar  in  that  situation  and 
obtained  fluid.  This  was  dis- 
tinctly bloody  in  appearance 
and  so  surprised  the  operator 
that  after  ixn-mitting  an  ounce 
or  two  to  flow  he  withdrew  his 
cannula  for  the  purpose  of  dis- 
cussing the  significance  of  the 
blood.  We  concluded  it  was  a 
hu'morrhagic  effusion,  and  ad- 
vised a  fresh  tapi)iiig.  This 
was  now  objected  to  by  the 
])are)its  on  the  ground  that 
once  at  a  time  was  enough, 
and  a  repetition  of  the  |)rocedure  was  deferred.  It  was  never 
repeated,  however,  and  because  of  the  following  considerations: 


'Jl. — 'I'lIK   VAIilors   SiTi;-    I'.i:    I'l   \.    II  i;l' 

IV  Paisacentesis  Pekicardii. 

Dotted  line  indicates  course  of  interniil  main 

mary  artery. 


PERICARDITIS  WITH   EFFUSION  95 

The  great  obstacle  to  absorption  was  believed  to  lie  in  the  enor- 
mous congestion  within  the  portal  system,  and  the  boy's  dis- 
tress was  due  not  so  much  to  pressure  from  the  effusion  as  to 
the  extreme  stasis  within  the  abdomen.  Tapping  the  pericar- 
dium might  relieve  the  heart,  but  with  all  the  conditions  pres- 
ent in  the  mitral  regurgitation  for  the  maintenance  of  hepatic 
engorgement  it  could  not  materially  improve  the  state  of  things 
in  the  portal  system.  Consequently,  with  the  heart-muscle  show- 
ing no  very  threatening  signs  of  failure,  it  was  thought  best  to 
make  one  last  vigorous  onslaught  on  the  stasis  within  the  hepatic 
vessels.  Accordingly  a  drachm  of  the  saturated  solution  of 
Epsom  salts  was  ordered  hourly  until  it  began  to  exert  effect. 
At  the  same  time  a  drachm  of  the  fresh  infusions  of  digitalis 
made  from  English  leaves  was  prescribed  every  four  hours.  The 
results  were  astonishing.  Several  doses  of  the  magnesia  sul- 
phate were  taken  next  morning  without  any  very  marked  effects 
upon  the  bowels,  but  instead  the  kidneys  began  to  act,  and  in 
the  next  twenty-four  hours  diuresis  amounted  to  something  like 
8  quarts.  Islot  only  did  the  patient's  dyspnoea  lessen,  but  the 
area  of  cardiac  dulness  began  promptly  to  diminish  in  size,  the 
liver  became  softer  and  less  tender,  and  the  patient's  improvement 
was  clearly  noticeable  even  to  his  parents.  The  salts  were  con- 
tinued daily,  though  with  gradually  diminishing  amounts.  After 
two  or  three  days  sirup  of  squills  was  added  to  the  infusion  of 
digitalis,  and  the  progress  towards  recovery  continued  without  in- 
terruption. This  little  patient  lived  nearly  three  years,  and  then 
died  from  a  fresh  pericarditis,  with  signs  of  dilatation,  but  not 
effusion. 

Some  are  sceptical  concerning  the  efficacy  of  medicinal  treat- 
ment in  promoting  absorption,  basing  their  objections  on  the  fact 
that  absorption  sometimes  sets  in  spontaneously,  even  after  the 
pericardial  effusion  has  remained  stationary  for  some  time. 
Nevertheless,  in  this  case,  the  change  for  the  better  began  so  soon 
after  the  administration  of  the  magnesium-salt  that  I  believe  it 
can  be  justly  regarded  as  an  instance  of  propter  hoc,  not  post  hoc. 
Unfortunately,  the  result  of  therapeutic  measures  is  not  always  so 
brilliant  as  was  this.  The  effusion  persists  in  spite  of  hydragogue 
cathartics  and  diuretics,  or  the  exudation  takes  place  so  rapidly 
and  copiously  that  it  threatens  to  overpower  the  heart  before  time 


96  DISEASES  OF   THE  HEART 

is  allowed  for  remedies  to  exert  their  effect.  In  either  event  the 
pericardium  ought  to  be  tapped,  and  it  is  best  not  to  delay.  It 
seems  to  me  there  can  be  no  question  concerning  the  indication 
for  paracentesis  in  such  cases,  but  early  in  the  disease  I  see  no 
call  for  surgical  interference  so  long  as  alarming  pressure-symp- 
toms do  not  supervene. 

Sites  for  Puncture. — Properly  performed,  this  operation  is 
safe,  and  as  it  is  likely  to  afford  prompt  relief,  one  should  always 
stand  ready  to  tap  whenever  such  intervention  is  indicated.  The 
indications  are  not  always  found  in  dyspnoea,  cyanosis,  and  rapid- 
ity of  the  pulse;  these  symptoms  are  present  in  all  cases  of  peri- 
cardial effusion  of  considerable  amount,  but  indications  are  present 
whenever  the  heart  shows  evidence  of  dangerous  weakness  by  syn- 
copal attacks  and  intermittence,  or  when  sufficient  time  having 
been  given  for  spontaneous  recovery,  or  for  absorption  through 
medicinal  treatment,  these  do  not  take  place.  Paracentesis  being 
decided  on,  it  only  remains  to  select  a  suitable  point  for  punc- 
ture. Various  sites  (see  Fig.  :21)  are  recommended,  and  all  aim 
at  reaching  the  fluid  most  readily  without  fear  of  w^ounding  the 
heart,  internal  mammary  artery,  or  other  structures. 

The  point  most  usually  recommended  is  in  the  fifth  left  inter- 
costal space  at  a  safe  distance  from  the  internal  mammary  artery. 
As  this  passes  downward  from  7  to  ^  inch  from  the  edge  of  the 
sternum,  the  needle  may  be  introduced  either  very  close  to  the 
sternal  border,  so  as  to  be  between  it  and  the  vessel,  or  at  the  outer 
side  of  the  artery  1  inch  or  more  from  the  bone.  Potch  pre- 
fers the  fifth  right  interspace  close  to  the  sternum,  since  at  this 
point  the  sac  is  sure  to  be  distended,  even  should  the  amount  of 
fluid  prove  smaller  than  is  anticipated.  Shattuck  has  ])unctured 
in  the  fifth  left  S])ace,  1  to  2  inches  outside  the  ni]iple-line,  just 
witliin  the  left  lateral  border  of  cardiac  dulness,  where,  as  a  mat- 
ter of  fact,  I  advised  ta])ping  in  the  case  narrated,  although  at  the 
time  I  was  not  aware  of  Shattuck's  recommendation.  The  objec- 
tion urged  against  this  site  is  the  possibility  of  wounding  the 
pleura  at  this  point.  Tliis  is,  of  course,  a  cogent  reason,  yet  if 
the  sac  is  greatly  distended  it  will  have  ])ushed  the  border  of  the 
left  lung  well  aside,  and  the  pericardium  will  occupy  the  region 
normally  filled  by  the  lung.  In  my  case  fluid  was  readily  reached, 
and  the  surgeon  was  confident  he  did  not  touch  the  pleura.     An- 


PERICARDITIS  WITH  EFFUSION  97 

other  point  at  which  the  sac  can  often  be  safely  pierced  in  cases 
of  extensive  effusion  is  in  the  angle  between  the  left  margin  of  the 
xiphoid  cartilage  and  the  adjacent  costal  cartilages.  The  fluid 
tends  to  gravitate  to  the  bottom  of  the  sac,  and  consequently 
weighs  down  the  diaphragm  and  left  lobe  of  the  liver,  so  that  if 
the  needle  is  thrust  upw^ard  and  backward  there  is  very  little 
danger  of  wounding  the  diaphragm.  For  additional  particulars 
concerning  paracentesis,  as  well  as  incision  of  the  pericardium, 
the  reader  is  referred  to  works  on  surgery. 

Whether  all  the  effusion  possible  is  to  be  withdrawn,  or 
whether  only  a  portion,  sufficient  to  lessen  the  pressure  and  favour 
subsequent  absorption  of  the  remainder,  is  a  matter  that  must  oe 
left  to  the  judgment  of  the  operator.  Personally,  I  advocate  the 
removal  of  the  whole  or  of  as  much  as  can  be  taken  without  danger 
of  the  heart  coming  in  contact  with  the  point  of  the  needle. 

Theoretical  considerations  suggest  the  expediency  of  following 
the  operation  by  the  administration  of  diuretics  and  heart-tonics. 
The  latter  include  digitalis  and  its  congeners,  which  sustain  and 
strengthen  the  heart-muscle  while  at  the  same  time  they  increase 
pressure  in  the  renal  artery,  and  thus  re-enforce  any  other  diu- 
retic remedies.  The  emplojanent  of  such  agents  serves  to  deplete 
visceral  congestion  and  to  thus  enhance  the  benefit  derived  from 
the  withdrawal  of  the  fluid  which  is  the  original  cause  of  the  stasis. 

The  treatment  of  purulent  effusion  should  be  surgical.  Should 
the  nature  of  the  primary  infection  and  symptoms  of  more  or  less 
pronounced  septicaemia  suggest  that  the  pericarditis  is  suppura- 
tive, the  character  of  the  exudate  should  be  determined  by  explora- 
tory puncture,  and  if  this  prove  to  be  pus,  it  should  be  evacuted 
without  delay  in  accordance  with  proper  surgical  methods.  Lil- 
ienthal,  of  l^ew  York,  reported  before  the  JSTew  York  Academy  of 
Medicine  a  case  of  suppurative  pericarditis,  occurring  in  a  lad 
who  was  recovering  from  pneumonia,  affecting  three  lobes.  Eight- 
een ounces  of  pus  w^ere  withdrawn  at  the  time  of  the  exploratory 
puncture,  and  40  more  at  the  time  the  sac  was  cut  down  upon  and 
opened.  The  pus  contained  numerous  pneumococci.  The  tem- 
perature had  been  irregularly  intermittent.  Complete  recovery 
followed  the  operation.     Eucaine  was  used  as  a  local  anaesthetic. 

Hcemorrhagic  effusion  is  to  be  managed  according  to  the  prin- 
ciples governing  the  treatment  of  the  sero-fibrinous  form,  no  spe- 


98  DISEASES  OF  THE   HEART 

cial  indication  for  treatment  being  presented  bj  the  bloody  charac- 
ter of  the  effusion.  Xo  great  effect  is  to  be  expected,  however, 
from  either  medical  or  surgical  treatment  in  those  cases  in  which 
the  affection  is  associated  with  a  serious  blood-state  or  djscrasia, 
and  measures  should  be  directed  to  the  removal  of  these  latter. 

The  subsequent  management  of  a  patient  convalescing  from 
acute  pericarditis  consists  in  such  measures  as  will  rapidly  restore 
the  general  health  and  heart-tone  in  the  hope  that  the  organ  may 
not  be  left  seriously  damaged.  We  possess  no  means  of  either 
preventing  adhesions  or  promoting  the  absorption  of  fibrinous 
deposits. 


CHAPTER    II 

CHRONIC    PERICARDITIS 

Syn.  :  Adherent  Pericardmm,  Synechia  Pericardii,  Concretio  Pericardii 
sen  Concretio  Cordis 

Chronic  pericarditis  may  be  divided  into  two  great  groups: 
(1)  That  in  which  it  involves  only  the  two  layers  of  the  sac,  peri- 
carditis interna  chronica,  and  (2)  that  in  which  the  process  in- 
volves both  the  pericardium  and  mediastinum,  pericarditis  in- 
terna et  externa  chronica.  In  both  of  these  forms  inflammation 
results  in  the  formation  of  fibrous  tissue,  which  binds  the  parts 
more  or  less  closely  and  extensively  together.  There  is  still  an- 
other much  rarer  form  in  which  the  chronic  inflammation  is  asso- 
ciated with  serous  distention  of  the  sac,  and  is  termed  therefore 
chronic  pericarditis  with  effusion. 

Adherent  pericardium  is  the  term  most  commonly  applied  by 
English  writers  to  the  first  form,  while  the  second  is  known  as 
chronic  adhesive  {s.  fihroiis,  s.  indurative)  niediastinopericarditis. 
Adherent  pericardium  has  long  been  recognised  by  pathologists, 
but,  owing  to  the  difficulty  of  its  diagnosis,  escaped  clinical  recog- 
nition, although  it  is  a  comparatively  frequent  post-mortem  find- 
ing. Out  of  86  cases  of  heart-disease  examined  after  death  at 
St.  Mary's  Hospital  from  1890  to  1893,  there  were,  according  to 
John  Broadbent,  31  instances  of  adherent  pericardium. 

Although,  according  to  Roberts,  Sir  Samuel  Wilks  had  fre- 
quently called  attention  both  pathologically  and  clinically  to  the 
existence  of  chronic  fibrous  thickening  within  the  mediastinum 
and  involving  the  pericardium,  chronic  indurative  mediastino- 
pericarditis  was  first  systematically  described  by  Kussmaul  in 
1873.  In  1894  Harris,  of  Manchester,  added  another  valuable 
contribution  to  the  subject  and  collected  all  the  published  cases. 
Eor  much  of  what  will  be  said  in  the  following  pages  I  wish  to 

99 


100  DISEASES   OP  THE   HEART 

express  acknowledgnieiiT  to  Harris's  monogra])h,  and  to  thank- 
fully acknowledge  the  stininliis  derived  therefrom.  It  has  en- 
abled me  to  give  more  intelligent  and  discriminating  study  to  the 
cases  which  have  come  to  my  notice.  I  now  systematically  look 
for  indications  of  chronic  mediastinopericarditis,  and  discover 
them  many  times  when  otherwise  I  should  probably  have  over- 
looked them.  Unfortunately,  ante-mortem  observations  of  several 
pronounced  cases  have  been  nuide  in  which  post-mortem  corrobora- 
tion of  the  diagnosis  has  been  denied.  Several  instructive  and 
typical  instances  will  be  narrated  in  these  pages.  I  wish  also  to 
express  my  indebtedness  to  John  Broadbent's  monograph  on  this 
subject,  as  well  as  to  Friedel  Pick's  paper,  Pericarditic  Pseudo- 
cirrhosis  of  the  Liver,  in  which  is  particularly  discussed  the  effects 
on  the  liver  and  the  production  of  ascites. 

Morbid  Anatomy. — The  morbid  anatomical  changes  found 
in  chronic  j^ericarditis  are  almost  always  the  result  of  previous 
acute  inflammation.  The  more  common  form  is  the  result  of  the 
organization  of  the  fibrinous  exudate  of  an  ordinary  silastic  peri- 
carditis. This  process  nuiy  begin  as  early  as  the  third  or  fourth 
day  of  the  acute  inflammation.  It  is  essentially  a  conservative 
process,  tending  to  make  good  the  damage  wrought  by  the  inflam- 
mation. This  is  brought  about  by  the  conversion  of  the  inflam- 
matory exudate  into  a  granulation-tissue,  and  finally  into  fibrous 
cicatrical  tissue. 

The  deeper  layers  of  the  exudate  are  first  invaded  by  newly 
forming  blood-vessels  and  connective-tissue  cells  with  many  leuco- 
cytes, which  form  the  granulation-tissue.  This  gradually  grows 
into  and  replaces  the  entire  exudate,  and  in  the  course  of  time  the 
development  of  intercellular  substance  converts  it  into  the  glisten- 
ing, white  cicatrix.  If  during  this  process  the  two  layers  of  the 
pericardiuiji  arc  in  contact,  union  takes  })lace  and  the  cicatriza- 
tion produces  firm  adhesion  between  the  opposing  surfaces.  These 
adhesions  mux  be  general  or  local,  varying  with  the  extent  of  the 
original  process,  and  with  the  conditions  obtaining  at  the  time  of 
organization  of  the  exudate. 

When  the  adhesion  is  circumscribed  it  is  most  frequently 
found  in  tlie  parts  of  the  sac  where  the  motion  is  the  least,  most 
frequently,  then,  at  the  base  of  the  heart,  about  the  great  vessels, 
less  often  at  the  a])ex  oi-  at  the  l)orders  of  the  organ.     When  adhe- 


CHRONIC  PERICARDITIS  101 

sion  does  not  occur,  the  formation  of  scar-tissue  produces  glisten- 
ing white  areas  on  the  surface  of  the  heart,  which  show  where 
the  previous  inflammation  existed.  These  are  the  so-called  milk- 
spots  or  inaculcE  tendinice. 

An  intermediate  condition  between  this  and  the  synechia  peri- 
cardii, or  completely  adherent  pericardium,  is  that  shown  when 
slight  circumscribed  adhesions  have  been  partially  or  completely 
torn  apart  by  the  motion  of  the  heart,  producing  string-like  pro- 
cesses of  fibrous  tissue  that  may  connect  the  two  surfaces,  or  may, 
in  rare  cases,  hang  loose  in  the  pericardial  sac.  When  the  layers 
are  not  adherent,  in  rare  cases  fluid  is  found  in  the  sac. 

The  layers  of  the  pericardium  may  be  adherent  with  but  slight 
thickening,  but  it  is  the  rule  to  find  considerable  increase  in 
fibrous  tissue,  especially  in  the  chronic  tuberculous  form,  where 
it  may  become  extreme. 

Calcification  may  occur,  especially  following  a  purulent  peri- 
carditis, the  pus  becoming  first  inspissated,  and  then  impregnated 
with  lime-salts.  Such  calcareous  plates  may  be  isolated,  or  may 
form  a  complete  investment  for  the  heart,  resembling  a  coat  of 
mail  (Ziegler).  In  this  case  the  motion  of  the  heart  is  permitted 
by  cracks  and  fissures  in  the  calcareous  mass. 

Chronic  pericarditis  is  often  associated  with  chronic  endocar- 
ditis, for  the  reason  that  they  both  often  have  the  same  rheumatic 
origin.  Moreover,  chronic  valvular  disease  seems  to  predispose 
to  pericardial  inflammation. 

Secondary  to  the  pericarditis  are  usually  found  more  or  less 
hypertrophy  and  dilatation  of  the  heart,  with  degeneration  of  the 
myocardium,  which  probably  are  the  result  of  the  mechanical  hin- 
drance to  the  heart's  action,  and  also  of  the  visceral  changes  that 
are  always  the  result  of  long-standing  circulatory  disturbance. 

Also  associated  with  the  chronic  pericarditis  may  be  an  indura- 
tive mediastinitis.  It  may  exist  alone,  but  its  more  frequent  oc- 
currence in  combination  with  indurative  pericarditis  renders  it 
appropriate  to  consider  it  here.  It  consists  of  a  more  or  less  ex- 
tensive hyperplasia  of  the  connective  tissue  of  the  mediastinum, 
which  binds  together  the  structures  contained  therein,  and  is  often 
associated  with  adhesion  of  the  two'  layers  of  the  pericardium. 
This  development  of  fibrous  tissue  results  either  from  an  extension 
of  a  chronic  pericarditis  through  the  parietal  layer  of  the  peri- 


102  DISEASES  OF  THE  HEART 

cardium,  or  from  a  chronic  proliferative  inflammation  of  the  me- 
diastinum itself,  either  alone  or  associated  with  pericarditis.  Ex- 
tensive fibrons  adhesions  may  bind  the  heart-sac  inseparably  to 
the  diaphragm,  or  the  sac  may  be  united  to  the  anterior  chest-wall,, 
to  the  pleura',  (jesophagus,  spinal  column,  or  to  all  these  structures. 
In  some  instances  the  contents  of  the  mediastinum  are  so  matted 
together  by  dense  fibrous  tissue  that  they  cannot  be  separated 
without  laceration  of  the  organs. 

When  such  extensive  adhesions  exist  they  may  be  found  to 
form  but  a  part  of  a  chronic  inflammatory  or  proliferative  process 
which  has  led  to  extensive  or  general  adhesions  between  the  two 
layers  of  the  pleura,  or  between  the  lungs  and  the  diaphragm. 

In  exceptional  cases  fibrous  adhesions  have  formed  only  at  the 
roots  of  the  great  vessels,  and  have  led  to  partial  or  complete  oblit- 
eration of  the  superior  vena  cava,  either  alone  (Roberts),  or  in. 
combination  with  involvement  of  the  main  trunk  of  the  pulmo- 
nary artery,  or  the  ascending  aorta  (Kussmaul).  At  the  present 
writing  I  have  under  observation  a  female  patient,  in  whom,  to 
judge  from  physical  signs,  chronic  mediastinopericardial  adhe- 
sions have  led  to  such  i-etraetion  of  the  borders  of  the  lungs  that 
the  entire  anterior  surface  of  the  heart  is  uncovered.  The  apex- 
beat  is  held  immovably  fixed  in  the  seventh  intercostal  space, 
anterior  axillary  line.  The  normal  excursion  movements  of  the 
diaphragm  in  front  are  entirely  abolished,  and  the  respiration  is 
of  purely  costal  type. 

The  secondary  effects  of  this  form  of  the  disease  are  not  lim- 
ited to  the  heart,  as  in  the  simple  adherent  pericardium.  As  the 
disease  is  usually  combined  wath  chronic  valvular  disease,  it  is 
difficult  to  say  how  much  importance  is  to  be  attached  to  this,  and 
how  much  to  the  fixation  of  the  pericardium  in  the  production  of 
the  great  hypertrophy  and  dilatation  found  in  these  cases.  The 
changes  in  the  lungs  of  chronic  broncliitis  and  brown  induration 
are  due  partly  to  the  passive  hypeni'mia  secondary  to  the  cardiac 
disease,  and  partly  to  the  retraction  and  immobility  of  the  lungs 
incident  to  the  pleuro-pericardial  or  associated  pleuritic  adhesions. 

Cirrhosis  of  the  liver  is  generally  present,  and  is  largely  re- 
sponsible for  the  ascites  so  frequently  observed  as  a  terminal  event. 
There  may  be  also  thickening  and  contraction  of  the  capsule  of 
the  liver  and  spleen,  and  more  or  less  evidence  within  the  abdom- 


CHRONIC  PERICARDITIS  103 

inal  cavity  of  what  appears  to  have  been  a  general  serositis  or  pro- 
liferative inflammation  of  the  serous  membranes. 

Chronic  Pericarditis  ivith  Effusion. — This  form  of  pericardial 
disease  is  but  rarely  encountered;  when,  however,  it  does  exist, 
it  may  be  considered  to  have  originated  in  one  of  two  ways:  (1) 
It  may  start  as  an  acute  attackj  which,  instead  of  undergoing 
complete  subsidence,  suffers  repeated  exacerbations,  and  finally 
merges  into  a  chronic  inflammatory  process.  (2)  In  consequence 
of  the  mildness  of  the  infection  the  pericarditis  assumes  a  slowly 
progressive  character  from  the  beginning,  at  no  time  manifesting 
a  tendency  to  undergo  arrest.  In  the  former  class  the  exudation 
fluctuates  in  amount  from  time  to  time,  according  as  the  intensity 
of  the  inflammation  abates,  and  partial  absorption  occurs,  or  ac- 
cording as  fresh  infection  occurs  the  inflammatory  process  again 
rekindles.  In  the  second  class,  chronic  from  the  outset,  effusion 
accumulates  slowly,  and  either  remains  stationary,  after  having 
reached  a  certain  degree,  or  tends  to  gradually  increase.  This 
form  of  chronic  pericarditis  is  said  to  be  observed  chiefly  in 
elderly  or  aged  individuals,  and  to  be  associated  with  chronic 
nephritis.  Roberts  expresses  the  opinion  that  such  cases  can  be 
differentiated  only  Avith  great  difiiculty  from  instances  of  hydro- 
pericardium,  and  that  it  is  quite  jDossible,  indeed,  that  the  chronic 
pericarditis  originated  in  a  simple  serous  transudation.  This,  it 
seems  to  me,  is  quite  unlikely  unless  the  originally  serous  effusion 
becomes  infected  by  pus-cocci,  in  which  event  it  would  likely  be 
transformed  into  pyopericardium. 

Etiology. — Chronic  pericarditis  is  in  most  instances  of  either 
rheumatic  or  tuberculous  origin,  the  inflammation  having  been 
slowly  progressive  from  the  start.  In  other  cases  an  acute  process 
passes  into  a  chronic  one,  which  exhibits  no  tendency  to  abate- 
ment, but  persists  for  years  with  repeated  exacerbations  of  the 
inflammation.  This  is  the  case  particularly  with  the  form  which, 
starting  in  the  sac,  spreads  to  the  mediastinum,  and  ultimately 
becomes  a  chronic  fibrous  mediastinopericarditis. 

In  some  cases  a  mediastinitis  is  first  set  up  and  subsequently 
invades  the  pericardium.  This  last  form  may  originate  as  either 
a  chronic  or  acute  mediastinitis,  which  is  set  up  by  disease  of  the 
bronchial  or  mediastinal  glands,  malignant  tumours,  tuberculosis 
of  the  lungs,  pleura  or  glands,  pneumonia,  or  by  trauma. 


104  DISEASES   OF  THE   HEART 

The  disease  is  most  frequently  observed  in  young  adults  and 
in  children.  Of  22  cases  collected  by  Harris  in  which  autopsy 
was  held,  only  2  occurred  in  persons  past  thirty,  while  9  were 
under  eighteen  years  of  age.  Several  instances  have  been  re- 
ported of  its  post-mortem  discovery  in  infants.  According  to  Har- 
ris, chronic  indurative  mediastinopericarditis  is  much  more  fre- 
quent in  males  than  females,  20  out  of  25  cases  having  belonged 
to  the  former  sex. 

Symptoms. — Many  cases  of  adherent  pericardium  run  an 
absolutely  latent  course,  and  are  only  discovered  on  the  autopsy 
table.  In  other  cases  the  symptoms  are  those  of  circulatory  and 
respiratory  embarrassment,  and  are  attributed  to  dilatation  or  to 
an  associated  valvular  disease.  In  a  third  series  of  cases  the 
synechia  pericardii  is  overlooked  owing  to  the  development  of 
ascites  and  other  symptoms  of  hepatic  cirrhosis.  For  the  most 
part  the  last-mentioned  class  of  cases  belongs  to  what  has  been 
described  as  chronic  adhesive  mediastinopericarditis. 

The  explanation  of  these  clinical  differences  is  not  always 
clear,  but  probably  depends  upon  several  factors.  If  the  pericar- 
dial adhesions  are  of  limited  extent  they  may  produce  no  appre- 
ciable secondary  effects  on  the  heart  or  circulation,  but  if  they 
lead  to  total  obliteration  of  the  sac,  and  particularly  if  this  latter 
is  also  bound  to  some  of  the  surrounding  structures,  cardiac  hyper- 
trophy is  likely  to  result,  which,  if  slight,  is  not  recognised  clinic- 
ally and  does  not  occasion  symptoms  of  embarrassed  circula- 
tion. If,  however,  the  heart  is  dilated  as  well  as  hypertrophied, 
it  is  very  apt  to  be  more  or  less  inadequate  with  resulting  respira- 
tory and  circulatory  symptoms.  The  enlargement  of  the  organ 
may  be  recognised,  but  not  its  cause,  and  the  condition  is  perhaps 
considered  cardiac  myasthenia  or  even  chronic  myocarditis. 

Sir  William  Broadbent  is  of  the  opinion  that  pericardial  adhe- 
sions load  most  frequently  to  enlargement  of  the  right  heart  in 
conseciueiice  of  the  relative  thinness  of  its  wall,  Avhile  others  main- 
tain that  tlie  entire  lieart  is  hyix-i'trophied.  The  mode  of  produc- 
tion of  hyj)ertrophy  in  cases  of  adherent  pericardium  is  difficult  of 
satisfactory  explanation,  but  is  due  in  some  way  to  the  hampering 
of  the  heart's  work. 

In  most  instances  conditions  are  prescMit  which  easily  account 
for  the  cardiac  hypertroj)liy.     Chronic  valvnhir  disease  and  adher- 


CHRONIC  PERICARDITIS  105 

ent  pericardium  coexist,  or  the  heart  is  restricted  in  its  function 
by  adhesions  between  it  and  surrounding  parts  (chronic  adhesive 
mediastinopericarditis).  In  still  other  instances  the  effects  of  a 
valve  lesion  are  intensified  by  mediastinopericardial  adhesions. 
In  any  case  the  pericarditis  either  prevents  the  establishment  of 
adequate  compensation  or  occasions  premature  loss  of  such  com- 
pensation as  may  have  been  attained. 

When  symptoms  eventually  appear  they  may  be  such  as  are 
seen  in  uncomplicated  but  uncompensated  valvular  defects ;  ve- 
nous stasis,  hepatic  and  other  visceral  engorgement,  oedema,  as- 
cites, dyspnoea,  and  cough  with  or  without  expectoration,  which 
may  be  simply  catarrhal  or  bloody,  according  to  the  degree  of  pul- 
monary congestion. 

In  some  cases  wdthout  coexisting  valvular  disease  the  earli- 
est symptoms  are  palpitation,  either  with  or  without  dyspnoea, 
called  forth  by  effort  or  excitement,  and  occasion  much  discom- 
fort and  alarm.  In  such  the  pulse  is  apt  to  be  habitually  rapid, 
while  cardiac  impulse  is  exaggerated  in  force  and  extent.  In 
other  cases,  again,  circulatory  disturbance  is  shown  by  digestive 
disorders,  lasting  for  many  years  and  attributed  to  simple  dys- 
pepsia or  chronic  gastritis,  but  never  traced  to  their  proper 
source  because  of  its  obscurity  or  impossible  diagnosis  of  the  peri- 
cardial adhesions.  In  all  such  cases  there  is  nothing  to  distin- 
guish them  from  ordinary  instances  of  cardiac  incompetence  due  to 
dilatation  or  mitral  disease. 

Physical  examination  usually  discloses  hepatic  enlargement, 
and  if  signs  of  heart-disease  are  not  apparent  the  condition  is 
thought  to  be  cirrhosis  of  the  liver,  either  hypertrophic  or  atro- 
phic, according  to  the  degree  of  enlargement  and  density  or 
smoothness  of  the  organ. 

In  cases  of  adherent  pericardium  displaying  pronounced  en- 
gorgement of  the  liver,  I  have  been  impressed  by  its  peculiar  ob- 
stinacy to  treatment.  The  hepatic  congestion  is  most  difficult  of 
reduction  by  ordinary  methods,  and  displays  a  striking  tendency 
to  recur  so  soon  as  treatment  is  abandoned. 

For  several  years  I  have  had  in  charge  a  patient  whose  mitral 
valve  leaks  and  whose  enormously  enlarged  heart  is  apparently 
completely  incased  in  fibrous  tissue  that  binds  down  the  organ  on 
all  sides,  so  that  no  amount  of  rest  in  bed  or  digitalis  seems  to 


106  DISEASES   OF   THE   HEART 

reduce  its  size  in  the  least.  The  liver  has  always  been  greatly 
engorged,  extending  for  a  long  time  nearly  to  the  crest  of  the 
ileum,  and  requiring  the  daily  use  of  saline  laxatives  to  relieve 
the  patient  from  pain  and  discomfort.  For  the  past  year  the 
organ  has  been  gradually  diminishing  somewhat  in  size  and  in- 
creasing in  thinness  and  hardness.  The  patient  has  experienced 
remarkably  little  dyspnoea  on  effort,  but  is  greatly  annoyed  by  the 
pounding  and  tumultuous  action  of  the  heart,  this  sensation  being 
specially  noticeable  in  the  epigastrium.  Of  late,  she  has  had 
a  great  deal  of  cough,  difficult  mucous  expectoration,  and  upon 
several  occasions  slight  haemoptysis.  She  has  to  be  extremely 
careful  in  her  diet,  and  her  urine  and  menses  have  become 
scanty. 

Another  female  patient  with  pronounced  mitral  insufficiency 
has  pericardial  adhesions  that  bind  down  the  left  side  and  base  of 
the  heart,  fixing  the  apex-beat  immovably  in  place,  far  to  the  left 
and  downward,  but  the  border  of  the  right  heart  is  apparently 
free  from  adhesions.  Whereas  the  left  ventricle  never  varies  in 
size  under  any  conditions,  the  right  heart,  as  shown  by  the  area 
of  cardiac  dulness,  becomes  dilated  with  the  greatest  ease  and 
rapidity.  The  liver,  which  is  ])ersistently  enlarged,  fluctuates 
somewhat  in  size  in  accordance  with  the  state  of  the  right  heart, 
but  even  when  at  its  smallest  always  extends  from  2  to  3  inches 
below  the  inferior  costal  margin,  no  matter  how  vigorous  may  be 
the  onslaughts  upon  it  by  means  of  Epsom  salts.  This  patient's 
symptoms  are  not  of  the  digestive  organs,  but  are  those  of  short- 
ness of  breath  and  a  rapid  pounding  action  of  the  heart  and  gen- 
eral weakness.  The  urine  remains  fairly  abundant,  and  the 
menses  are  too  profuse  and  protracted.  She  is  always  promptly 
benefited  by  absolute  rest  in  bed,  a  milk  diet,  cathartics,  and  digi- 
talis, although  this  last-named  agent  never  materially  slows  the 
heart. 

The  most  interesting  class  of  cases  are  tliose  whose  clinical  fea- 
tures closely  resemble  a  case  of  atrophic  cirrhosis  of  the  liver. 
These  cases,  usually  of  chronic  fibrous  mediastinopericarditis, 
generally  pursue  a  latent  course  for  many  years,  and  often,  even 
after  symptoms  have  set  in,  are  not  recognised  as  adherent  peri- 
cardium until  they  come  to  autopsy.  Not  only  is  there  a  chronic 
engorgement  of  the  liver,  l)iit  there  is  a  perihepatitis  with  increase 


CHRONIC  PERICARDITIS  107 

of  the  interstitial  connective  tissue.  In  time  this  fibrous  tissue, 
undergoing  contraction,  causes  a  reduction  in  size  and  marked 
increase  in  the  hardness  of  the  liver,  which,  extending  below  the 
costal  arch  to  a  variable  distance,  feels  thin,  dense,  and  regular, 
the  notch  being  intensified,  and  often  one  lobe  disproportionately- 
larger  than  the  other.  It  is  now,  when  the  organ  has  shrunken 
and  grown  dense,  that  symptoms  begin.  The  patient's  attention 
is  first  attracted  by  an  increase  in  the  size  and  firmness  of  his 
abdomen.  In  some  instances  icterus  accompanies  or  even  pre- 
cedes this  increase  of  girth. 

At  length  driven  to  seek  medical  advice,  he  is  discovered  to 
have  slight  icterus  and  ascites,  usually  without  oedema  of  the  lower 
extremities.  The  physican  examines  the  heart  and  urine,  detects 
no  heart-disease  and  discovers  no  albumin,  but  perhaps  some  bile. 
The  case  is  put  down  as  one  of  hepatic  cirrhosis.  The  following 
is  an  illustrative  case : 

A  man  of  fifty-five,  who  had  been  intensely  jaundiced  for  near- 
ly two  years,  and  in  August,  1900,  was  tapped  for  ascites,  called 
me  in  consultation  a  short  time  ago.  The  ascites,  which  had  for  a 
time  been  reduced  by  apocynum  cannabinum,  only  to  speedily 
recur,  had  been  again  drawn  off  the  morning  of  the  day  I  saw  him. 
He  had  had  articular  rheumatism  eighteen  years  before,  but  had 
suffered  no  shortness  of  breath  or  other  discomfort  since.  The 
thin-bordered,  dense,  slightly  granular-feeling  liver  extended  in 
the  median  line  nearly  to  the  umbilicus  and  from  one  costal  arch 
to  the  other,  being  lost  beneath  the  right  ribs,  just  outside  the 
right  mamillary  line.  Owing  to  the  recent  paracentesis,  the  peri- 
toneal cavity  was  free  from  fluid,  and  there  was  no  cedema.  The 
cardiac  area  was  somewhat  increased  to  the  right  and  downward, 
the  sounds  were  clear  and  strong  and  free  from  murmurs.  The 
rather  tapping  apex-beat  was  in  the  fifth  left  interspace  inside  the 
vertical  nipple-line,  and  there  was  a  distinct  though  feeble  pulsa- 
tion in  the  epigastrium.  In  the  fifth  and  sixth  interspaces,  be- 
tween the  apex-beat  and  sternum,  and  also  in  the  sulcus  between 
the  ensiform  appendix  and  adjacent  costal  cartilages,  a  systolic  re- 
traction could  be  perceived  both  by  palpation  and  inspection. 
Furthermore,  when  the  patient  was  instructed  to  take  a  slow,  deep 
breath,  the  right  external  jugular  could  be  seen  to  bulge  out  during 
the  inspiratory  effort.     This  distention  was  also  palpable.     Pulsus 


108 


DISEASES  OF  THE   HEART 


paradoxus  could  not  be  detennined.  I  had  no  hesitation  in  mak- 
ing a  diagnosis  of  pseudo-atrophic  cirrhosis  of  the  liver  secondary 
to  an  adherent  pericardium.  This  patient  died  a  few  weeks 
later. 

One  of  the  most  typical  cases,  and  by  the  way  the  first  of  the 
kind  I  ever  saw,  was  seen  in  1801  with  Dr.  Christophe.  The 
patient  was  a  male,  aged  fifty-two,  had  always  enjoyed  good  health 
until  an  attack  of  the  grip  in  February,  1880,  after  Avhich  his 
health  failed  progressively.  Six  weeks  prior  to  my  visit  he  took 
to  the  house  with  dropsy  and  ascites.  The  former  yielded  to  caf- 
feine and  digitalis,  but  the  latter  persisted  until  drawn  off  by  tap- 
ping the  day  before  I  saw  him.  The  patient  was  in  bed,  of  medi- 
um height,  considerably  emaciated,  and  complained  of  dyspncea, 

dry  cough,  anorexia,  flatu- 
lence, constipation,  scanty  non- 
albuminous  urine,  pain  in  the 
hepatic  region,  and  insomnia. 
The  lungs  were  negative, 
but  on  examining  the  heart 
the  apex-beat  was  found  to  be 
a  weak  tap  in  the  fifth  left  in- 
terspace on  the  nipple-line  and 
to  be  followed  by  a  distinct 
diastolic  rebound  or  shock, 
while  there  was  in  addition  an 
unmistakable  systolic  reces- 
sion of  the  fifth  interspace, 
from  the  border  of  the  ster- 
num to  a  point  outside  of  the 
apex-impulse.  Cardiac  dul- 
ness  extended  from  the  right  sternal  border  to  ^  an  inch  outside 
the  left  nipple,  and  in  the  mitral  area  was  a  harsh  systolic  mur- 
mur that  was  transmitted  to  mid-axillary  line  (Fig.  '22).  Both 
heart-sounds  were  audible,  and  the  socoiid  at  the  apex  was  followed 
by  a  short  diastolic  murmur.  The  inferior  hepatic  border  was 
palpable  2  inches  below  the  costal  arch,  and  was  thin,  hard,  and 
somewhat  irregular.  The  ])ulse  was  slow,  tense,  and  regular,  and 
there  was  no  icterus. 

The  diagnosis  was  jdainly  that  of  mitral  regurgitation  and 


Location  of  Border  of  Liver. 


CHRONIC   PERICARDITIS  109 

adherent  pericardium  with  secondary  cirrhosis  of  the  liver  and 
ascites. 

The  chronicity  of  such  a  case  is  attested  by  the  fact  that  after 
repeated  tappings  and  prolonged  confinement  to  the  house  this 
patient  again  appeared  in  public,  and  was  accidentally  encoun- 
tered by  me  in  the  fall  of  1895.  He  admitted  that  he  was  not  very 
well,  and  that  he  still  had  his  ascites.  He  died  a  few  months  sub- 
sequently. In  this  interesting  case  cardiac  symptoms  did  not  as- 
sert themselves,  and  the  clinical  history  was  essentially  that  of 
atrophic  cirrhosis  of  the  liver,  and  would  ordinarily  pass  for  such. 

The  following  case  is  narrated  because  of  its  interesting  clini- 
cal course  and  instructive  pathological  findings:  ]\Irs.  M.,  aged 
forty-five,  consulted  me  in  February,  1S93,  because  of  an  obsti- 
nate cough  which  had  developed  the  J^ovember  previous  and  re- 
sisted treatment.  She  gave  a  history  of  scarlatina  at  the  age  of 
seven,  and  of  a  pain,  probably  rheumatic,  in  the  right  hip  almost 
continually  betw^een  her  tenth  and  thirteenth  years.  She  stated, 
also,  that  at  that  time  she  suffered  from  shortness  of  breath  upon 
attempting  to  run  or  go  upstairs,  and  at  such  times  had  an  inclina- 
tion to  faint.  She  thought  her  pulse  had  always  been  irregular, 
since  whenever  she  had  had  occasion  to  require  the  services  of  a 
physican  comment  was  made  upon  its  irregularity.  She  was  mar- 
ried at  the  age  of  twenty-one,  and  two  years  later  gave  birth  to  her 
only  child,  both  the  pregnancy  and  labour  having  been  uneventful, 
excepting  for  a  mild  "  milk  leg."  Fourteen  years  subsequently 
she  became  a  widow.  She  had  considered  herself  well  except  for 
nervousness  and  attacks  of  neuralgia.  In  the  fall  of  1892  was 
treated  for  pain  and  swelling  of  right  leg,  between  ankle  and 
knee,  and  for  "  fulness  and  tightness  "  about  the  waist.  In  iSTo- 
vember  had  contracted  a  bronchitis,  and  since  then  had  not  been 
free  from  cough,  although  under  treatment  for  same. 

Her  only  symptoms  at  the  time  she  consulted  me  were  fre- 
quent paroxysmal  cough,  with  scanty  mucous  expectoration,  pain 
across  the  chest,  in  consequence  of  the  cough,  and  moderate  short- 
ness of  breath  on  exertion.  Digestion,  bowel  movements,  and  mic- 
turition seemed  normal.  She  had  passed  the  menopause  several 
months  before. 

She  was  5  feet  1  inch  in  height  and  weighed  145  pounds. 
The  pulse  was  103,  somewhat  irregular,  not  intermittent,  small, 


110  DISEASES   OF   THE   HEART 

and  weak.  The  lungs  were  resonant  throughout,  and  the  breath- 
sounds  vesicular ;  no  rales  except  line  inspiratory  crepitus  at  the 
extreme  right  base,  close  to  the  spinal  column,  and  at  the  extreme 
lower  limit  of  the  left  lung,  from  the  anterior  axillary  to  the  pos- 
terior scapular  line.  These  rales  were  thought  to  indicate  old 
pleuritic  adhesions.  The  apex-beat  was  in  the  fifth  left  space  2 
inches  from  the  sternum,  broad,  strong,  and  at  times  thumping. 
There  was  slight  epigastric  pulsation,  and  cardiac  dulness  was 
increased  somewhat  to  the  right. 

The  pulmonic  second  sound  was  accentuatedj  while  the  first 
at  the  apex  was  at  times  split  and  thumping,  at  times  preceded  by 
a  short,  rough  presystolic  murmur.  A  systolic  apex-murmur  was 
not  very  distinct.  Xo  signs  of  adherent  pericardium  were  noted 
at  that  time  either  because  overlooked,  or  because  the  chronic  me- 
diastinitis  did  not  develop  until  a  year  or  two  subsequently.  The 
lower  border  of  the  liver,  firm  and  rounded,  was  palpable  nearly 
at  the  level  of  the  umbilicus.     There  was  no  oedema. 

The  diagnosis  was  made  of  mitral  stenosis  in  a  fair  state  of 
compensation,  secondary  hepatic  engorgement,  and  chronic  bron- 
chitis, probably  secondary  also  to  the  mitral  disease. 

Under  appropriate  treatment,  directed  mainly  to  relieving 
stasis  in  the  pulmonic  and  general  venous  systems,  cough  gradu- 
ally disappeared,  and  the  patient  considered  herself  in  fair  health 
during  the  summer.  In  May  it  was  noted  that  the  pulse  was  100, 
not  intermittent,  but  slightly  irregular  in  force.  The  following 
October,  after  I  had  returned  from  Bad  Xauheim,  and  instituted 
the  balneological  treatment  of  heart-disease  in  my  practice,  the 
patient  decided  to  try  a  course  of  baths.  For  a  time  they  seemed 
to  benefit  her,  but  after  about  three  weeks  she  said  she  began  to 
notice  increase  in  the  size  of  her  abdomen  at  its  lowest  part.  I  at 
once  examined  her,  and  to  my  surprise  detected  unmistakable 
signs  of  moderate  ascites.  The  baths  were  discontinued  in  the 
belief  that  inasmuch  as  they  had  not  prevented  the  development 
of  ascites,  they  would  not  cause  its  removal. 

From  that  time  onward  ascites  gradually  increased  until  in 
June,  1894,  paracentesis  was  performed  for  the  first  time.  From 
this  time  to  the  date  of  her  death,  a  period  of  three  years,  the 
fluid  was  drawn  off  32  times,  the  longest  interval  between  the  tap- 
pings being  seven  weeks  and  the  shortest  six  days.     In  addition 


CHRONIC  PERICARDITIS  111 

she  took  elaterin  in  large  doses  and  various  diuretic  remedies. 
Palpation  of  the  liver  now  showed  that  it  had  become  thin,  very 
hard,  and  deeply  notched. 

About  two  years  before  her  death  she  began  to  suffer  from 
what  appeared  to  be  attacks  of  subacute  bronchitis.  At  such 
times  there  was  mild  continuous  pyrexia  and  the  cough  was  most 
harassing,  often  effectually  preventing  sleep  and  requiring  large 
doses  of  codeine  phosphate.  All  known  expectorants  in  various 
combinations  were  tried  with  apparently  no  more  effect  than  to 
facilitate  expectoration.  The  only  treatment  that  seemed  of  ma- 
terial benefit  was  truly  heroic  catharsis,  since  the  withdrawal  of 
the  ascites  seemed  only  to  remove  pressure  on  the  diaphragm,  but 
not  to  lessen  the  great  venous  engorgement. 

These  attacks  grew  more  frequent,  the  intervals  between  them 
shorter,  until  at  last  cough  became  chronic  and  persisted  to  the 
end.  During  these  months  I  saw  her  but  rarely,  as  her  son,  who 
was  a  physician,  devoted  himself  to  her  care.  At  one  of  my  visits, 
a  year  or  more  before  her  death,  I  discovered  fine  crackling  rales 
all  around  the  base  of  the  right  lung,  particularly  in  front,  which 
were  brought  out  distinctly  by  deep  inspiration,  and  were  un- 
changed by  cough.  These  rales  eventually  spread  so  as  to  be  heard 
nearly  to  the  clavicle,  while  as  time  went  on  similar  crepitant 
sounds  became  audible  more  or  less  extensively  at  the  base  of  the 
left  lung.  They  did  not  seem  to  have  the  characters  of  pleuritic 
friction,  and  I  was  at  a  loss  to  explain  them.  It  may  here  be 
stated,  however,  that  the  autopsy  subsequently  showed  them  to 
have  been  due  to  wide-spread  pleuritic  adhesions. 

A  year  before  her  death  her  son  first  detected  systolic  reces- 
sion of  the  intercostal  space,  close  to  the  site  of  the  apex-beat, 
and  pulsus  paradoxus.  Bacilli  were  never  discovered  in  the  spu- 
tum, and  repeated  examinations  of  the  urine  showed  nothing 
more  than  the  usual  changes  due  to  passive  congestion.  The  last 
months  of  life  were  spent  in  a  continual  struggle  to  keep  within 
reasonable  limits  the  ever-present  and  never-conquerable  venous 
engorgement.  (Edema  of  the  lower  extremities  supervened  many 
weeks  before  the  end,  which  finally  took  place  in  May,  1897, 
with  symptoms  closely  resembling  but  not  identical  with 
uraemia. 

Thanks  to  the  intelligent  study  of  the  case  by  her  son,  the  ante- 


112  DISEASES  OF  THE   HEART 

mortem  diagnosis  was  made  of  chronic  indurative  mediastino- 
pericarditis.  !Xo  other  signs  ever  developed  than  the  few  men- 
tioned above,  pulsus  paradoxus  and  a  visible  s;v'stolic  recession  in 
immediate  proximity  to  the  apex. 

The  autopsy  was  made  by  Dr.  W.  A.  Evans  twenty-seven  hours 
after  death,  and  was  briefly  as  follows :  The  abdomen  contained  a 
small  amount  of  fluid,  and  the  omentum  was  adherent  to  the  ab- 
dominal wall  above  the  umbilicus  and  along  the  linea  alba,  adhe- 
sions being  so  firm  that  they  could  not  be  separated  without  tear- 
ing the  omentum.  The  uterus  was  larger  than  normal,  the  right 
tube  very  firmly  adherent  to  rectum  and  posterior  part  of  the 
uterus,  right  ovary  being  normal ;  left  tube  also  firmly  adher- 
ent to  the  left  side  of  the  rectum  and  side  of  pelvis  and  posterior 
wall  of  the  uterus,  completely  covering  the  left  ovary,  which  was 
also  normal.  There  was  an  exudate  upon  the  anterior  surface  of 
the  left  broad  ligament.  The  liver  was  adherent  to  the  abdominal 
wall  over  both  right  and  left  lobes,  the  ])arietal  layer  of  the  peri- 
tona'um  being  thickened  and  its  visceral  layer  showing  evidence  of 
old  inflammation.  The  organ  measured  9  by  5  inches,  its  right 
lobe  4  inches  vertically,  and  its  left  lobe  2  inches  in  its  antero- 
posterior diameter.  The  surface  of  the  liver  was  markedly  irregu- 
lar and  divided  by  scars  into  large  areas,  its  lower  border  being 
so  notched  that  it  was  practically  impossible  to  make  out  the 
lobes.  Its  capsule  was  irregularly  thickened,  presenting  the  ap- 
pearance of  lace-work.  The  substance  of  the  organ  was  firm,  cut- 
ting with  resistance,  and  the  lobules,  very  irregular  in  size,  stood 
out  prominently,  and  the  connective  tissue  of  the  capsule  could 
be  traced  into  the  underlying  liver  substance^ — in  short,  it  was  in  a 
state  of  advanced  Glissonian  cirrhosis. 

The  right  kidney,  5]  inches  long  and  2^  wide  and  2  thick, 
showed  increase  in  the  thickness  of  its  capsule,  some  parenchym- 
atous degeneration  and  interstitial  overgrowth.  The  left  kid- 
ney, 5  by  3  by  If  inches,  with  capsule  firmly  adherent  in  places 
and  thickened,  showed  other  changes  the  same  as  in  right  kidney. 

The  spleen  showed  marked  tliickening  and  some  interstitial 
splenitis. 

The  gastro-intestinal  tract  showed  no  especial  changes,  except 
that  the  peritoneal  covering  was  thickened. 

The  appendix  was  firmly  bound  down  to  the  right  iliac  fossa 


CHRONIC  PERICARDITIS  113 

by  a  solid  mass  of  adhesions  behind  the  caecum,  and  was  less  than 
1  inch  in  length. 

The  right  pleural  cavity  was  the  seat  of  very  extensive  adhe- 
sions, which  were  most  firm  anteriorly  and  more  abundant  at  the 
apex  than  at  the  base.  There  was  considerable  fluid  in  this  cavity, 
and  the  lung  was  firmly  attached  to  the  diaphragm.  The  pulmo- 
nary pleura  was  thickened,  and  on  section  the  surface  of  the  lung 
showed  considerable  anaiimia,  no  tuberculous  nodules,  and  no  in- 
flammation. 

The  left  lung  was  adherent  at  base  anteriorly  and  also  poste- 
riorly, adhesions  to  diaphragm  being  very  solid.  At  apex  was  a 
superficial  calcareous  mass  attached  to  the  visceral  pleura,  and  in 
other  respects  the  left  lung  was  of  the  same  appearance  and  con- 
dition as  the  right  lung. 

The  pericardium  w^as  attached  to  the  pleurae  and  chest-wall, 
and  m  situ  felt  like  a  solid  bony  shield,  reaching  to  the  sixth  rib 
and  ^  an  inch  within  the  left  mammary  line.  Upon  removal  of 
the  heart  it  was  found  that  the  organ  was  completely  incased  by 
several  calcareous  plates,  which  were  closely  in  apposition  with 
yet  separated  from  each  other,  so  that  the  lines  of  separation  had 
allowed  the  heart  to  undergo  contraction  and  relaxation.  These 
plates  of  lime  united  the  two  pericardial  layers  firmly.  The  walls 
of  the  several  chambers  were  hypertrophied,  particularly  the  left 
auricle  and  right  ventricle.  With  exception  of  the  left  ventricle 
the  cavities  were  all  moderately  dilated.  The  heart-muscle  had 
the  appearance  of  brown  atrophy.  All  valves  excepting  the  mitral 
were  healthy,  these  being  thickened,  stiffened,  adherent  along 
their  edges,  and  projected  into  the  cavity  of  the  ventricle  like  a 
cone  or  funnel.  The  mitral  orifice  was  moderately  thickened  with 
old  sclerotic  tissue  and  admitted  one  finger. 

To  me  it  is  very  interesting  and  quite  remarkable  that  the  pa- 
tient was  never  able  to  give  any  history  of  an  attack  of  pericar- 
ditis, which  the  necropsy  showed  must  have  been  very  extensive. 
It  probably  occurred  at  so  early  a  period  in  childhood,  perhaps 
subsequent  to  the  scarlatina,  that  it  failed  to  be  impressed  on  her 
memory,  or  was  not  discovered  at  the  time.  If  it  was  secondary 
to  the  scarlet  fever,  forty-one  years  elapsed  before  it  finally  led 
to  the  patient's  death.  The  post-mortem  findings,  furthermore, 
revealed  in  a  striking  manner  the  extent  to  which  chronic  pro- 


114  DISEASES  OF  THE   HEART 

liferative  inflammation  may  involve  other  structures,  notably  the 
liver,  and  may  lead  ultimately  to  the  clinical  features  of  hepatic 
cirrhosis  with  ascites.  The  adhesive  inflammation  of  the  pleurae 
probably  occurred  at  the  time  when  the  j)atient  manifested  a  low 
grade  of  fever  with  cough,  and  fine,  dry  crepitus  over  the  front 
and  base  of  the  right  lung,  and  subsequently  also  of  the  left.  This 
case  also  illustrates  the  chronicity  of  some  of  these  cases,  and  the 
fact  that  death  is  the  result  not  so  much  of  cardiac  asthenia  as  of 
the  effect  on  the  system  of  the  associated  conditions.  That  etio- 
logical data  in  such  cases  are  frequently  wanting,  and  that  there- 
fore the  primary  cause  of  the  symptoms  may  be  unsuspected  to  the 
end,  is  shown  by  tlie  following  case : 

Mrs.  D.,  a  physician's  wife,  aged  forty-six,  was  first  seen  by 
me  December  24,  1894,  because  of  .increasing  symptoms  of  cardiac 
disease.  Her  statements  were  positive  that  with  the  exception 
of  measles  and  whooping-cough  in  childhood  she  had  never  been 
ill  before  the  onset  of  her  present  trouble.  She  had  been  a  school- 
teacher up  to  her  marriage  three  years  before.  Her  husband 
stated  that  he  at  first  noticed  tachycardia  shortly  after  marriage, 
but  no  other  symptoms  had  been  observed  until  May,  1894.  She 
then  developed  dyspnoea  on  exertion,  and  occasionally  oedema  of 
the  lower  extremities  and  face.  During  the  summer  of  1894  she 
took  sulphate  of  strychnine,  digitalis,  strophanthus  "  off  and 
on  "  without  apparent  benefit,  but  had  recently  shown  some  im- 
provement on  iodide  of  potash  and  belladonna.  Her  menses 
were  absent  since  July ;  the  only  symptoms  complained  of  were 
slight,  dry  cough,  a  not  very  marked  breathlessness  on  exertion, 
a  feeling  of  weakness,  and  occasional  puffiness  of  the  lower 
extremities. 

She  was  of  medium  height  and  well  nourished.  Examination 
discovered  signs  of  fluid  in  the  right  pleural  cavity,  reaching  to 
the  lower  angle  of  the  scapula,  and  some  fine  crackling  nlles  at 
the  extreme  posterior  left  base  that  grew  more  abundant  after 
cough. 

Otherwise  tlie  lungs  were  negative.  The  pulse  was  small, 
weak,  regular,  and  moderately  accelerated.  The  apex-beat  was  in 
the  fifth  left  interspace,  just  outside  the  nipple-line,  diffused  and 
weak.  There  was  no  epigastric  pulsation,  but  at  the  level  of  the 
fourth  costal  cartilage  deep-seated  cardiac  dulness  reached  from  1 


CHRONIC   PERICARDITIS 


115 


inch  to  the  right  of  the  sternum  to  fully  midway  between  the  left 
nipple  and  the  anterior  axillary  line  (i'ig.  23).  There  were  no 
murmurs,  but  the  first  sound  at  the  apex  was  weak  and  the  second 
at  the  base  reduplicated,  the  pulmonic  second  being  accentuated. 
'No  signs  of  adherent  pericarditis  were  noticed.  The  lower  hepatic 
border  was  palpable  at  the  level  of  the  umbilicus,  and  was  thin 
and  hard.     The  spleen  was  not  enlarged,  and  there  was  no  ascites. 

The  case  was  considered 
one  of  general  cardiac  dilata- 
tion supervening  upon  a  previ- 
ous hypertrophy  of  the  left 
ventricle  and  upon  the  in- 
creased pulmonary  blood-pres- 
sure occasioned  by  the  fluid 
in  the  right  pleural  cavity. 
How  much  of  the  increase 
in  heart's  dulness  to  the  left 
was  attributable  to  dilatation, 
and  how  much  to  transposi- 
tion of  the  organ  from  pres- 
sure by  the  intrapleural  fluid, 
was  left  an  open  question.  In 
the  absence  of  a  definite  his- 
tory of  pleurisy  and  of  other 
signs  of  dropsy,  the  nature  of 
the  liquid  in  the  pleural  cavity,  whether  an  exudate  or  transudate, 
was  a  matter  of  doubt.  The  liver  was  evidently  cirrhotic.  Exam- 
ination of  the  urine  was  negative. 

In  spite  of  physical  rest,  digitalis,  diuretics,  and  cathartics, 
the  amount  of  intrapleural  fluid  remained  stationary  for  the  next 
three  weeks.  Paracentesis  was  then  performed,  and  the  fluid  rap- 
idly reaccumulating,  the  operation  was  repeated  within  a  Aveek. 
After  the  second  aspiration  the  fluid  mounted  to  the  upper  level 
of  the  third  rib  and  symptoms  of  pressure  increased.  It  was  then 
decided  to  try  the  efficacy  of  baths  (Bad  Xauheim).  These  were 
endured  so  badly,  however,  that  they  were  discontinued  after  four 
days.  By  February  6tli  the  actual  embarrassment  had  become  so 
pronounced  that  this  fact,  together  with  the  failure  of  paracen- 
tesis to  permanently  reduce  the  amount  of  pleural  effusion,  led  the 


Fig.  23. — Showing  Apex-beat,  Cakdiac 
Dulness,  and  Liver  Border  in  Case 
(p.  114). 


116  DISEASES  OP  THE  HEART 

consulting  surgeon  to  advise  resection  of  a  rib  in  the  hope  that 
jDermanent  drainage  would  afford  time  and  opportunity  for  the 
heart  to  regain  its  former  vigour.  The  proposal  having  been  laid 
before  the  patient  and  her  husband,  and  their  consent  obtained, 
the  operation  was  done  the  next  day.  Everything  seemed  to  pro- 
gress favourably  for  a  few  days,  when  suddenly  symptoms  of  pro- 
nounced fibrinous  pleuritis  developed  in  that  side.  Temperature 
rose  to  102°  F.,  strength  waned  rapidly,  and  the  patient  died  ten 
days  after  the  operation.  I  may  say  here  that  the  infection  was 
subsequently  proved  to  be  a  pneumococcus  one. 

The  autopsy  was  made  by  Dr.  Hektoen  twenty-four  hours  after 
death,  and  the  findings  may  be  briefly  stated  to  have  been  a  totally 
adherent  pericardium,  with  several  plates  of  lime-salts  upon  the 
surface  of  the  ventricles,  the  largest  lamina  being  about  the  size 
of  a  silver  half  dollar.  The  sac  was  also  bound  by  adhesions  to  the 
left  pulmonary  pleura,  but  not  to  the  chest-wall.  The  valves  and 
myocardium  seemed  normal,  there  was  evidence  of  recent  right- 
sided  pleurisy  with  collapse  of  the  lung,  and  acute  oedema  of  the 
left  lung  with  some  fresh  diaphragmatic  pleurisy  on  that  side. 

The  liver  was  cirrhotic,  but  not  atrophied.  Kidneys  were 
healthy,  and  there  were  evidences  of  perihepatitis  and  peri- 
splenitis. 

The  necropsy  seemed  to  make  it  evident  that  the  condition 
within  the  right  pleural  cavity  had  been  a  hydrothorax,  while  the 
pericardial  adherence  explained  why  medical  treatment  had  been 
unavailing.  Had  this  patient  lived,  and  time  been  afforded  for 
shrinkage  of  the  liver  to  take  place,  ascites  would  undoubtedly 
have  developed,  and  the  case  have  presented  the  clinical  features 
of  what  Pick  terms  pericarditic  pseudocirrhosis  of  the  liver,  the 
same  as  did  the  others. 

In  explanation  of  ascites  in  such  cases  Heideman  lays  down 
the  four  following  propositions:  (1)  In  these  cases  there  is 
chronic  inflammation  of  all  the  serous  membranes.  (2)  The  stag- 
nation occasioned  by  degeneration  of  the  cardiac  muscle  leads  to 
ascites,  because  on  account  of  the  chronic  peritonitis  the  peritoneal 
vessels  offer  a  locus  minoris  resistentice.  (3)  The  cirrhotic  pro- 
cess in  the  liver  so  often  observed  under  these  circumstances  is  oc- 
casioned by  extension  of  the  inflammatory  irritation  from  the 
capsule  of  the  liver  as  well  as  by  the  chronic  hyperaemia.      (4) 


CHRONIC   PERICARDITIS  117 

Bv  the  growth  and  contraction  of  this  connective  tissue  in  and 
about  the  liver  the  stagnation  and  transudation  in  the  abdominal 
cavity  are  increased. 

Course  and  Termination.- — The  course  of  chronic  adhesive 
pericarditis  varies  much,  depending  upon  the  extent  of  the  adhe- 
sions and  the  coexistence  or  not  of  other  diseases,  as  chronic 
valvular  lesions.  If  the  process  is  confined  to  obliteration  of  the 
sac  the  condition  may  last  for  many  years,  and  the  patient  subse- 
quently die  from  some  independent  affection.  Usually,  however^ 
the  same  as  when  mediastinopericarditis  leads  to  extensive  union 
with  the  surrounding  parts,  the  disease,  after  having  persisted  for 
a  long  time  without  symptoms,  is  likely  to  bring  about  those  cir- 
culatory and  respiratory  disturbances  already  described,  and  so 
well  illustrated  by  the  foregoing  cases.  If  adherent  pericardium  is 
associated  with  valvular  disease  it  affects  the  latter  injuriously, 
and  its  more  rapid  course  is  inseparably  connected  with  that  of  the 
endocardial  lesion.  In  such  a  case  cardiac  breakdown  is  inevita- 
ble, and  not  likely  to  be  long  postponed.  Xevertheless,  even  here 
much  depends  upon  the  treatment  and  upon  the  patient's  intelli- 
gent appreciation  of  his  condition.  In  the  case  of  the  young  lady 
whose  mitral  insufficiency  is  sadly  complicated  by  adhesion  of  the 
left  side  of  the  heart  and  apex  to  the  retracted  lung-border  and 
chest-wall,  symptoms  of  right  ventricle  failure  came  on  only  three 
years  after  her  first  attack  of  rheumatism,  and  were  undoubtedly 
hastened  by  the  pericardial  adhesions  (see  page  106).  It  is  now 
nearly  eighteen  months  since  her  symptoms  became  alarming,  and 
the  fact  that  her  overburdened  right  ventricle  is  to-day  actually 
doing  better  work  than  a  year  ago  is  due  to  the  persistent  use  of 
appropriate  remedies  and  to  her  having  learned  that  so  soon  as  the 
first  signal  of  danger  is  perceived  she  must  take  to  her  bed  until 
the  right  heart  recovers  its  tone. 

The  manner  in  which  many  cases  of  this  affection  terminate 
has  already  been  made  apparent.  Either  the  symptoms  are  those 
of  atrophic  cirrhosis  of  the  liver  or  they  are  indicative  of  cardiac 
insufficiency  of  mitral  disease.  Either  stasis  in  the  systemic  veins 
and  viscera  increases  until  the  patient  succumbs  to  general  exhaus- 
tion, or  in  another  set  of  cases  he  is  worn  out  after  months  or  years 
by  the  ever-recurring  ascites,  the  heart  not  evincing  special  weak- 
ness.    According  to  Kussmaul,  pulmonary  infarcts  are  particu- 


118  DISEASES  OF  THE   HEART 

larly  frequent  in  cases  of  chronic  mediastinopericarditis,  and 
these  may  prove  the  cause  of  death. 

Physical  Signs. — Inspection. — The  ease  and  certainty  with 
which  adherent  ])cricardiuni  can  be  recognised  clinically  depend 
upon  the  situation  and  extent  of  the  adhesions.  If  the  sac  is 
bound  down  to  the  heart,  but  not  to  surrounding  parts,  the  condi- 
tion does  not  of  a  necessity  produce  recognisable  physical  signs, 
and  this  fact  explains  why  sinechia  pericardii  is  so  often  first  de- 
tected on  the  post-mortem  table.  In  the  cases  in  which  an  adher- 
ent pericardium  is  diagnosed  there  are  generally  adhesions  be- 
tween the  sac  and  some  of  the  surrounding  structures,  as  the  ante- 
rior thoracic  wall,  the  pulmonary  pleura  on  either  side,  and  the 
diaphragm. 

Accordingly,  it  is  in  cases  of  chronic  indurative  mediastinoperi- 
carditis  that  the  diagnosis  is  most  easily  and  frequently  made.  This 
is  owing  to  the  fact  that  the  existence  of  adhesions  interferes  witb 
the  change  in  form  and  position  of  the  heart  normally  occasioned 
by  ventricular  systole.  During  this  phase  in  its  contractions  the 
heart  becomes  depressed  at  its  base,  and  assuming  a  more  rounded 
shape  thrusts  its  point  forward,  upward,  and  towards  the  left,  and 
thus  produces  the  impulse  against  the  chest-wall  known  as  the 
apex-beat. 

It  is  evident  that  if  adhesions  restrict  these  movements  the 
heart  will  of  a  necessity  pull  on  the  part  to  which  it  is  bound. 
This  pulling  action  is  exerted  during  ventricular  s3'stole,  and  con- 
sequently the  most  obvious  and  the  most  frequently  observed  sign 
of  adherent  pericardium  is  a  I'isihlc  systolic  recession  of  the  chest- 
wall.  It  may  be  perceived  in  various  situations,  but  most  com- 
monly in  the  neighbourhood  of  the  apex-beat.  Only  a  very  lim- 
ited area  may  be  thus  drawn  inward,  but  in  most  instances  a 
systolic  sinking  takes  i)lace  in  several  of  the  interspaces  near  the 
apex  and  even  in  the  e])igastrium,  the  extent  and  location  of  the 
adhesions  determining  tlie  extent  and  position  of  this  sign.  It  is 
best  observed  by  placing  the  patient  in  a  strong  light,  and  then 
looking  at  the  bared  chest  from  above  downward  or  from  one  side 
to  the  other. 

It  is  well  to  have  the  ])atient  suspend  respiration  for  a  mo- 
ment wliilc  inspection  is  being  iiiadc,  that  tlie  observer  may  not  be 
deceived  or  confused  by  sinking  of  the  soft  parts  incident  to  move- 


CHRONIC  PERICARDITIS  119 

ments  of  the  diaphragm.  Ordinarily,  there  is  but  slight  difficulty 
in  detecting  this  systolic  indrawing  in  question.  One  should  be 
careful,  however,  not  to  mistake  for  a  sign  of  pericardial  adhesions 
the  systolic  depression  that  sometimes  takes  place  in  the  third  and 
fourth  interspaces  close  to  the  left  border  of  the  sternum  in  cases 
of  great  cardiac  hypertrophy,  and  which  is  due  to  atmospheric 
pressure  as  the  base  and  body  of  the  heart  recede  from  the  chest- 
wall  during  systole. 

As  might  be  expected,  it  is  the  yielding  soft  parts  that  display 
systolic  retraction  most  readily,  and  as  it  is  possible  that  even 
near  the  apex  this  may  be  owing  to  atmospheric  jDressure,  this 
sign  is  not  jDathognomonic.  The  value  of  the  sign  is  far  greater, 
therefore,  when  the  ribs  and  end  of  the  sternum  are  drawn  inw^ard 
together  with  the  intersi3aces.  I  have  not  observed  this,  but  it 
is  said  to  sometimes  occur. 

Sir  William  Broadbent  first  described  a  systolic  retraction  of 
the  tenth  and  eleventh  interspaces  below  the  inferior  angle  of  the 
left  scapula  in  cases  of  adherent  pericardium,  and  hence  it  is  often 
spoken  of  as  Broadhenfs  sign.  It  is  occasionally  perceived  on  the 
right  side  also.  It  is  ascribed  to  the  drawing  on  the  diaphragm  of 
a  hypertrophied  and  powerfully  contracting  heart,  and  when  pres- 
ent is  considered  indicative  of  extensive  adhesions  between  the  sac 
and  the  diaphragm. 

Gibson  very  justly  attaches  great  importance  to  fixation  or  im- 
mobility of  the  apex.  J^ormally  the  heart,  and  hence  its  apex, 
gravitates  towards  the  dependent  side  whenever  the  patient  as- 
sumes either  lateral  decubitus.  When  he  lies  on  the  left  side  the 
point  of  the  heart  strikes  the  chest-wall  a  couple  of  inches  farther 
to  the  left  than  when  he  is  on  his  back,  while  in  the  right  lateral 
position  the  impulse  is  nearly  or  quite  behind  the  sternum,  and 
hence  imperceptible.  Consequently  in  any  case  in  which  this  mo- 
bility of  the  apex  is  not  observed,  it  is  suggestive,  nay  indicative, 
of  its  fixation  by  external  adhesions.  The  position  of  the  heart's 
apex  should  also  become  lowered  during  the  inspiratory  descent 
of  the  diaphragm,  striking  behind  the  sixth  costal  cartilage,  or 
even  the  sixth  interspace.  The  existence  of  adhesions  may  pre- 
vent this,  and  accordingly  fixation  of  the  apex  during  the  two  res- 
piratory acts  is  likewise  a  sign  of  adherent  pericardium. 

The  other  phenomena  perceived  by  inspection  in  some  cases 


120  DISEASES  OF  THE   HEART 

are  connected  with  the  external  jugular  veins,  and  are  (1)  in- 
spiratory swelling  of  the  veins,  known  as  KussmauVs  sign,  and 
(2)  diastolic  collapse  of  the  veins,  known  as  Friedreich's  sign. 
In  my  experience  these  signs  are  not  as  frequently  met  with  as  is 
the  drawing  inward  of  the  interspaces,  and  I  do  not  recall  an  in- 
stance of  diastolic  collapse  of  the  veins.  Kussmaul's  sign  is  pres- 
ent when  i^ericardial  adhesions  prevent  the  dilatation  of  the  right 
auricle  that  normally  takes  place  during  inspiration.  Instead  of 
the  inspiratory  act  exerting  an  aspirating  effect  upon  the  contents 
of  the  veins,  and  thus  collapsing  them,  the  opposite  effect  is  pro- 
duced, and  the  jugulars  become  visibly  distended.  Diastolic  col- 
lapse does  not  appear  to  l)e  limited  necessarily  to  the  jugulars,  since 
Broadbent  has  observed  it  in  the  superficial  veins  on  the  front  of 
the  chest,  and  says  it  was  due  to  traction  of  fibrous  bands  on  the 
coats  of  the  internal  mammary  vein  uniting  this  vessel  to  the  peri- 
cardium, and  causing  its  sudden  dilatation  during  ventricular  re- 
laxation. In  the  case  of  the  cervical  veins  their  diastolic  collapse 
is  probably  to  be  explained  by  the  aspiratory  force  exerted  by  the 
sudden  diastolic  rebound  of  the  right  auricle,  pulled  upon  as  it  is 
by  adhesions  between  it  and  surrounding  parts.  Two  other  physi- 
cal signs  that  remain  to  be  considered  are  best  perceived  by  the 
hand,  and  are  therefore  described  under  palpation. 

Palpation. — In  some  exceptional  instances  the  hand  laid  over 
the  apex  perceives  a  distinct  sudden  shock  not  synchronous  with 
systole,  but  with  diastole.  It  is  spoken  of,  therefore,  as  the  dias- 
tolic shock  or  rebound.  It  is  caused  by  the  pulling  of  fibrous  adhe- 
sions which,  put  on  the  stretch  during  systole,  pull  the  heart  sud- 
denly back  against  the  chest-wall  after  systole  has  ended.  Such  a 
rebound  can  scarcely  be  occasioned  by  any  other  condition  than  ex- 
ternal pericardial  adhesions,  and  therefore  by  some  is  considered 
pathognomonic  of  the  disease  under  discussion.  I  have  observed 
it  but  twice,  once  in  the  patient  whose  case  I  have  reported,  and 
the  other  time  in  a  man  at  Cook  County  Hospital  who  had,  in 
addition,  aortic  insufficiency. 

The  second  ])lienomenon  observable  1)V  palpation  is  tlio  pulsus 
paradoxus.  Normally  the  pulse  l)ecomes  fuller  and  stronger  to- 
wards the  end  of  inspiration,  smaller  and  weaker  towards  the  end 
of  expiration.  In  the  paradoxic  pulse,  on  the  contrary,  the  re- 
verse obtains,  strong  ins]>iration  causing  a  diminution  in  the  force 


CHRONIC   PERICARDITIS  121 

and  volume,  it  may  be  even  an  intermission  of  the  pulse,  while 
towards  the  close  of  expiration  the  pulse  regains  its  usual  strength 
and  fulness.  This  peculiarity  may  sometimes  be  perceived  in 
pericarditis  with  effusion,  and  therefore,  while  its  presence  serves 
to  corroborate  other  signs  of  adherent  pericardium,  it  in  nowise 
can  be  looked  upon  as  pathognomonic.  Aside  from  enabling  one 
■  to  appreciate  the  two  signs  just  mentioned,  palpation  is  of  service 
in  determining  the  mobility  or  fixation  of  the  apex  and  the  degree 
of  enlargement  and  density  of  the  liver — conditions  I  deem  of  con- 
siderable importance  in  doubtful  cases. 

Percussion. — This  is  of  great  value  in  all  cases  of  suspected 
or  known  heart-disease.  In  adherent  pericardium  cardiac  hyper- 
trophy or  dilatation  is  very  apt  to  exist,  and  hence  one  should  in 
every  suspected  case  attempt  by  percussion  to  ascertain  the  limits 
of  deep-seated  dulness,  since  in  the  absence  of  any  other  etiological 
factor  to  account  for  enlargement,  this  condition  would  point  to 
the  likelihood  of  adhesions. 

It  is  not  uncommon  in  cases  of  suspected  adhesions  for  the 
area  of  absolute  cardiac  dulness  to  be  increased  in  all  directions, 
particularly  upward  and  to  the  left.  This  may  be  due  to  a  simple 
crowding  aside  of  the  anterior  lung-margins  by  a  hypertrophied 
heart,  yet  the  borders  may  be  retracted  and  fixed  by  pleuropericar- 
dial  adhesions.  In  this  latter  condition  the  line  of  demarcation 
between  pulmonary  resonance  and  cardiac  dulness  is  unaffected  by 
respiratory  movements.  Therefore,  percussion  is  of  service  in 
enabling  one  to  determine  whether  or  not  the  lung-borders  are 
bound  down  by  adhesions. 

Auscultation. — For  the  most  part  this  is  of  negative  value, 
particularly  if  the  synechia  pericardii  is  not  associated  with  me- 
diastinopericarditis.  In  the  latter  condition  auscultation  some- 
times detects  fine  friction-rales  along  the  margins  of  the  lungs 
where  they  join  the  area  of  superficial  cardiac  dulness ;  and  if  such 
parchment-like  crackling  sounds  persist  during  the  cessation  of 
respiratory  movements,  they  furnish  strong  proof  of  the  existence 
of  pleuropericardial  adhesions. 

Roberts  quotes  Perez  as  authority  for  the  statement  that  in 

some  instances  of  chronic  mediastinopericarditis  a  creaking  sound 

upon  the  body  of  the  sternum  is  audible  during  up  and  down 

movements  of  the  arms.     I  have  tested  this  in  several  of  my  pa- 
10 


122  DISEASES   OF  THE   HEART 

tients,  and  in  two  I  detected  this  creaking  friction-sound  described 
by  Perez.  As  in  these  cases  other  positive  signs  of  adherent  peri- 
cardium were  present,  this  sign  of  Perez  possessed  considerable 
interest,  if  not  material  importance. 

Diagnosis. — From  the  foregoing  description  of  the  physi- 
cal signs  it  is  apparent  that  in  some  cases  the  diagnosis  of  peri- 
cardial adhesions  can  be  made  almost  at  a  glance,  while  in  others 
the  most  skilful  diagnostician  may  not  be  able  to  decide  whether 
the  pericardium  is  adherent  or  not.  The  difficulty  is  found  in 
cases  in  which  the  two  layers  of  the  sac  are  united  without 
adhesions  to  the  surrounding  parts.  In  such,  one  must  observe 
critically  the  jugular  veins  and  the  radial  pulse  in  the  hope  of 
detecting  some  of  the  anomalies  that  have  been  described.  The 
size  of  the  heart  should  also  be  mapped  out  by  percussion,  and  the 
liver  should  be  examined  as  to  its  size,  density,  and  outline,  since 
synechia  pericardii  may  declare  itself  by  no  other  signs  than  by  its 
eifect  on  these  organs. 

In  cases  of  chronic  indurative  mediastinopericarditis  the  mat- 
ter of  diagnosis  is  usually  far  less  difficult.  Indeed  there  may  be 
a  conjunction  of  several  physical  signs.  Thus  in  one  of  my  pa- 
tients the  apex  is  firmly  fixed  far  below  and  to  the  left  of  the 
nipple.  There  is  systolic  retraction  of  the  soft  parts  between  tlie 
apex  and  the  epigastrium,  and  of  the  intercostal  spaces  below  the 
left  scapula.  The  anterior  margins  of  both  lungs  are  drawn  aside 
and  immovable,  causing  nearly  the  whole  heart  to  be  uncovered, 
as  shown  by  the  great  area  of  superficial  dulness.  The  liver  ex- 
tends nearly  to  the  iliac  crest  and  is  hard  and  deeply  notched, 
while  owing  to  the  enormous  size  of  the  heart  and  liver  the  front 
of  the  chest  looks  distended  and  smooth,  and  when  the  patient 
stands  the  abdomen  appears  disproportionately  large  and  pendu- 
lous. Pulsus  paradoxus  and  inspiratory  swelling  of  the  cervical 
veins  are  also  present. 

Lastly,  one  should  always  be  suspicious  of  an  adherent  peri- 
cardium in  every  case  of  rheumatic  valvular  disease,  and  if  in  such 
a  case  the  liver  resembles  in  thickness  and  density  the  organ  in 
atrophic  cirrhosis,  yet  is  not  so  contracted,  if  ascites  develops 
without  apparent  cause,  or  takes  place  prior  to  or  out  of  propor- 
tion to  anasarca,  there  is  good  reason  to  suspect  the  complication 
of  an  adherent  pericardium. 


CHRONIC  PERICARDITIS  123 

The  differential  diagnosis  between  Laennec's  atrophic  cirrhosis 
of  the  liver  and  the  pericarditic  psendocirrhosis  just  considered 
is  often  the  most  difficult.  Aid  may  be  obtained  by  attention  to 
the  following  points:  (1)  In  Laennec's  cirrhosis  there  is  often  a 
history  of  alcoholism,  malaria,  or  syphilis,  while  in  the  other  form 
there  may  be  a  history  of  previous  pericarditis,  a  rheumatic  at- 
tack in  childhood,  or.  of  some  acute  illness  with  prsccordial  pain 
and  other  symptoms  suspicious  of  pericarditis.  (2)  In  Laennec's 
cirrhosis  ascites  develops  prior  to  anasarca,  whereas  in  the  variety 
now  considered  it  may  sometimes  follow  more  or  less  oedema  of  the 
lower  extremities  (Pick).  (3)  In  the  former  there  are  no  signs 
of  heart-disease,  while  in  the  latter  careful  examination  usually 
detects  enlargement  of  the  heart  either  alone  or  in  combination 
with  valvular  disease.  (4)  In  the  pseudo-atrophic  form  there  may 
be  some  of  the  signs  of  adherent  pericardium. 

Finally,  before  leaving  the  subject  of  diagnosis  of  chronic  peri- 
carditis, it  is  necessary  to  say  a  few  words  concerning  the  recogni- 
tion of  that  rare  form  in  which  the  chronic  inflammation  is  shown 
by  fluid  distention  of  the  sac.  In  this  variety  there  are  apt  to  be 
pressure-effects,  but  if  the  effusion  takes  place  insidiously  such 
effects  may  not  declare  themselves.  In  such  an  event  the  effusion 
is  usually  detected  accidentally,  or  if  discovered  its  true  nature  may 
not  be  suspected.  Roberts  cites  a  case  reported  by  Samuel  West 
of  the  existence  of  a  supposed  cyst  which  was  repeatedly  tapped 
during  life,  yet  which  after  death  was  found  to  be  a  chronic  peri- 
cardial effusion.  Unless  this  condition  is  observed  to  have  origi- 
nated acutely  its  diagnosis  must  depend  upon  percussion  and  aus- 
cultation evidences  of  distention  of  the  sac  in  accordance  with  the 
rules  laid  down  for  the  diagnosis  of  acute  pericarditis  with 
effusion. 

Prognosis. — If  pericardial  adhesions  occur  independently  of 
other  disease,  and  if  not  so  firm  or  extensive  as  to  materially  ham- 
per the  heart's  action,  they  may  in  nowise  affect  life  prospects. 
If,  on  the  contrary,  pericardial  synechia  is  complicated  by  a 
chronic  valve-lesion,  the  prognosis  is  unfavourable  as  to  great 
length  of  life.  If  the  heart  is  bound  down  more  or  less  completely 
to  the  surrounding  parts,  it  is  only  a  question  of  time  when  serious 
inadequacy  will  develop.  In  some  cases  the  adhesive  process  is 
stationary,  while  in  chronic  indurative  mediastinopericarditis  the 


124  DISEASES  OP  THE   HEART 

tendency  to  subsequent  adhesive  inflammation  of  other  serous 
membranes  and  to  the  spreading  of  the  adhesive  process  within 
the  mediastinum  furnishes  an  exceedingly  grave  outlook  for  the 
future.  When  ascites,  anasarca,  and  other  symptoms  of  the  final 
breakdown  appear  there  is  small  prospect  of  a  restoration  of 
compensation.  Under  such  conditions  the  duration  of  life  is  likely 
to  be  bounded  by  a  few  months  or  even  a  few  weeks.  Although,  as 
in  the  cases  narrated,  the  struggle  may  be  extended  over  a  number 
of  years,  the  patient  is  a  chronic  invalid  at  the  best,  and  can  only 
with  great  difficulty  postpone  the  fatal  event.  The  absence  of  all 
subjective  and  objective  symptoms  furnishes  presumptive  evi- 
dence that  the  adhesions  are  not  extensive.  If,  on  the  contrary, 
symptoms  of  engorgement  within  the  lesser  and  greater  circula- 
tion are  never  wholly  absent,  they  aflPord  the  basis  for  unfavourable 
prognosis.  The  greater  the  secondary  cardiac  hypertrophy  and 
dilatation,  particularly  in  children,  in  whom  chest  capacity  is 
small,  the  slighter  the  prospect  of  the  long  retention  of  adequate 
compensation.  When  the  last  stage  of  the  journey  is  reached  it  is 
likely  to  be  a  short  one. 

The  prognosis  of  chronic  pericardial  effusion  depends  upon 
its  etiology  and  the  length  of  time  during  which  it  has  existed.  It 
also  depends  upon  its  association  or  not  with  some  other  disease, 
as  chronic  nephritis,  and  upon  its  amenability  to  treatment. 

Treatment. — It  goes  without  saying  that  we  possess  no 
means  of  breaking  up  the  pericardial  adhesions ;  at  the  most  we 
can  only  strive  to  lessen  their  ill  effects  and  to  prevent. an  exten- 
sion of  the  process.  In  our  endeavour  to  accom]>lish  the  latter,  any 
rlieumatic  attack  or  acute  illness,  no  matter  how  trifling,  should 
be  promptly  and  energetically  combated  by  appropriate  means. 
The  patient  should  be  at  once  confined  to  the  house,  and  if  possi- 
ble to  the  bed,  in  order  to  relieve  the  heart  of  any  unnecessary 
work,  and  tlicreby  if  possible  pi-event  fresh  pericardial  inflamma- 
tion or  restrain  the  activity  of  the  process,  sliouhl  the  pericardium 
again  become  attacked.  Salicyhites,  counter-irritants,  or  other 
mild  antiphlogistic  measures  are  in  order. 

The  chief  aim  of  management  should  be  to  preserve  compen- 
satory hypertrophy,  and  so  far  as  possible  to  minimize  the  ill  ef- 
fects produced  by  the;  cai'diac  disorder.  In  my  opinion,  the  first 
essential  is  that  the  patient  be  not  left  in  absolute  ignorance  of 


CHRONIC   PERICARDITIS  125 

his  condition,  lest  lie  fail  to  grasp  the  full  importance  of  the  rules 
laid  down  for  his  guidance.  Most  individuals  are  greatly  alarmed 
by  being  told  they  have  heart-disease,  and  therefore  great  judg- 
ment and  tact  are  required  in  imparting  such  information.  If  the 
patient  has  no  suspicion  of  anything  being  wrong  with  his  heart, 
and  is  of  a  nervous,  excitable  temperament,  he  would  better  be  told 
only  a  part  of  the  truth.  It  may  be  stated  that  his  heart  is  not 
strong,  and  that  if  he  will  prevent  the  development  of  serious  trou- 
ble he  must  obey  certain  injunctions,  the  careful  observance  of 
which  will  i^reserve  his  health.  In  other  instances  the  whole  truth 
may  be  told  plainly,  but  in  a  manner  not  calculated  to  create  alarm. 
Only  in  this  way  can  we  expect  our  patients,  ignorant  of  physiol- 
ogy and  pathology,  to  avoid  harmful  efforts,  and  to  correct  injuri- 
ous habits. 

In  a  word,  a  heart  handicapped  by  extensive  adhesions,  and 
perhaps  also  by  serious  valve-disease,  must  not  be  given  more  work 
to  perform  than  it  is  capable  of  without  strain.  Inasmuch  as  what 
will  be  said  on  this  subject  in  the  chapters  devoted  to  the  treat- 
ment of  Valvular  Disease  in  General  is  applicable  to  the  aifection 
now  under  consideration,  the  reader  is  referred  to  those  chapters 
for  the  details  of  this  part  of  the  management. 

The  injurious  secondary  effects  of  adherent  pericardium  are 
not  limited  to  the  heart,  but  are  also  felt  by  the  organs  of  diges- 
tion and  elimination.  Congestion  within  the  portal  system  must 
be  diminished  from  time  to  time  by  the  administration  of  a  brisk 
cathartic.  The  patient,  and  even  the  physician,  often  rest  con- 
tent with  the  fact  that  the  bowels  move  regularly  every  day,  and 
lose  sight  of  the  benefit  derived  in  these  cases  from  periodically 
unloading  the  liver.  ISTothing  is  better  to  this  end  than  a  blue  pill 
or  a  grain  or  two  of  calomel,  followed  the  next  morning  by  a  glass 
of  some  saline  aperient  water.  The  patient  should  remain  under 
the  regular,  though  perhaps  not  very  frequent,  supervision  of  a 
physician,  who,  detecting  early  indications  of  cardiac  strain,  may 
promptly  meet  the  danger  by  ordering  an  appropriate  heart-tonic. 
Digitalis  and  strychnine  should  not  be  given  as  a  routine  practice, 
but  should  be  reserved  for  times  of  emergency. 

As  a  rule  the  symptoms  pointing  to  overstrain  on  the  part  of 
the  heart  can  be  allayed  by  regulation  of  the  diet,  restricting  the 
amount  of  work  or  exercise,  and  it  may  be  by  insisting  upon  rest 


126  DISEASES  OP  THE  HEART 

in  the  house  for  a  time.  The  food  should  be  relatively  rich  in 
proteids,  moderate  in  quantity,  and  taken  at  regular  intervals.  If 
the  individual  is  inclined  to  corpulence,  or  suffers  from  fermenta- 
tive indigestion,  carbohydrates  and  fats  should  be  allowed  spar- 
ingly. Unrestrained  consumption  of  fluids  is  objectionable,  since 
it  is  a  very  easy  matter  for  the  intake  of  liquids  to  greatly  exceed 
the  needs  of  the  system  and  the  eliminating  power  of  the  excretory 
organs. 

When  the  breakdown  of  compensation  at  length  comes,  with 
all  its  attendant  manifestations,  the  case  is  to  be  managed  in  ac- 
cordance with  the  principles  governing  the  treatment  of  the  same 
condition  in  any  other  form  of  cardiac  disease.  It  has  been  my 
experience  that  one  cannot  expect  or  achieve  as  brilliant  results 
from  the  employment  of  digitalis  in  these  cases  as  in  valvular 
affections  unfettered  by  adhesions.  It  is  not  so  much  a  question 
of  whipping  on  the  jaded  heart  as  it  is  of  relieving  it  of  as  much 
of  its  load  as  possible.  Physical  rest  must  be  strictly  enforced 
therefore,  and  catharsis  must  be  brisk.  Digitalis  must  be  given 
for  the  purpose  of  invigorating  rather  than  greatly  slowing  the 
heart,  and  with  a  view  of  obtaining  its  diuretic  effect.  Diuretin 
and  other  diuretic  remedies  are  also  in  order.  It  is  now  that 
strychnine  is  of  particular  service,  and  to  produce  its  most  bene- 
ficial effects  it  should  be  administered  hypodermically.  Pain, 
cough,  insomnia,  and  other  distressing  symptoms  are  to  be  relieved 
as  they  arise.  One  should  not  hesitate  to  remove  ascites  by  aspi- 
ration whenever  it  accumulates  to  the  extent  of  seriously  embar- 
rassing the  heart  and  respiratory  organs.  If  the  anasarca  does  not 
yield  to  appropriate  remedies,  it  may  be  drained  off  by  the  use 
of  Southey's  tubes  or  by  incising  the  ankles,  always  under  strict 
aseptic  precautions. 


CHAPTEE    III 

HYDROPERICARDIUM  —  H^^MOPERICARDIUM  —  PNEU- 
MOPERICARDIUM-TUBERCULOSIS  OF  THE  PERI- 
CARDIUM-SYPHILIS OF  THE  PERICARDIUM-CAR- 
CINOMA  AND    SARCOMA    OF   THE    PERICARDIUM 

I.    HYDROPERICARDIUM 

By  this  term  is  meant  a  transudation  of  serum  into  the  peri- 
cardial sac.  It  is  a  non-inflammatory  process,  and  the  analogue 
of  what  takes  place  under  similar  conditions  in  other  serous  cavi- 
ties. The  presence  in  the  pericardium  of  1  or  2  drachms  of  serum 
may  be  regarded  as  physiological ;  the  condition  is  pathological 
only  when  the  transudate  reaches  such  an  amount  as  to  constitute 
a  veritable  dropsy  (hydrops  pericardii).  Although  the  condition 
is  the  counterpart  of  transudation  into  other  serous  cavities,  it 
does  not  occur  with  anything  like  so  great  frequency  as  hydro- 
thorax  and  ascites. 

Morbid  Anatomy. — Upon  the  chest  being  open  the  pericar- 
dial sac  is  found  more  or  less  distended  and  fluctuating,  the  same 
as  in  pericarditis  with  effusion ;  a  great  difference  is  discovered, 
however,  when  the  sac  is  opened.  Instead  of  fibrin-masses  and 
other  evidences  of  inflammation,  together  with  a  serous  exudate, 
the  sac  contains  a  clear,  straw-coloured  fluid,  poor  in  albumin,  and 
containing  very  little  if  any  fibrin.  Because  of  its  relative  defi- 
ciency in  albumin  the  specific  gravity  of  the  transudate  is  lower 
than  that  of  a  sero-fibrinous  effusion,  ranging  from  1.008  to  1.015. 
The  pericardial  tissues  may  look  more  or  less  (Edematous;  but 
aside  from  this  appearance  and  being  filled  with  serum,  the  sac 
presents  nothing  worthy  of  note.  In  addition,  there  are  associated 
changes  in  other  tissues  and  organs — such  as  oedema,  depending 
upon  the  same  cause  as  the  hydropericardium ;  as  chronic  diseases 
of  the  heart  or  kidneys,  or  both,  which  have  served  to  bring  about 

137 


128  DISEASES  OF  THE   HEART 

the  serous  transiKlation  into  the  sac.  The  transudation  into  the 
pericardium  varies  in  amount  from  a  few  ounces  to  several 
pints. 

Etiology. — Ilydropericardium  is  a  dropsy,  and  therefore  is 
prodiu't'd  in  the  same  manner  and  depends  upon  the  same  variety 
of  causes  as  dropsical  fluid  in  other  situations.  The  causes  may 
be  divided  therefore  into  general  and  local.  The  general  include 
chronic  cardiac  disease,  nephritis,  both  acute  and  chronic,  and  ca- 
chexias. By  local  causes  are  meant  those  diseases,  such  as  tumours, 
Avhich,  sitmitcd  within  the  thorax,  exert  pressure  on  neighbouring 
blood-vessels,  and  thus  bring  about  stasis  in  the  veins  and  capil- 
laries of  the  pericardium.  Chronic  heart-disease  leads  to  dropsy 
in  the  same  way,  but  the  stasis  within  the  pericardial  vessels  is 
only  a  ])art  of  a  general  condition. 

Symptoms.  — These  are  likely  to  be  overshadowed  by  those  of 
dropsical  accumulation  in  the  pleural  cavity  and  general  venous 
congestion.  If  by  chance  hydropericardium  exists  alone,  a  very 
rare  event,  or  forms  the  leading  pathological  condition,  the  syni])- 
toms  are  those  resulting  from  pressure,  and  consist  of  the  same 
phenomena  of  circulatory  and  respiratory  embarrassment  as  are 
observed  in  cases  of  extensive  sero-fibrinous  pericarditis.  Dysp- 
noea is  more  or  less  marked,  and  may  even  amount  to  orthopnoea ; 
cyanosis  and  venous  congestion  are  also  present,  and  the  pulse  is 
small,  feeble,  rapid,  and  it  nuiy  be  irregular.  The  more  rapidly 
the  hydropericardium  supervenes  the  more  ])ronounced  the  symp- 
toms. As  dropsical  distention  of  the  sac,  when  it  develops  in  the 
course  of  chronic  cardiac  or  renal  disease,  is  one  of  the  terminal 
events,  it  (h've]o])s  so  slowly  that  sym])tonis  ai'c  likely  to  be  latent, 
and  tlierefore  e>ca))C  notice. 

Physical  Signs. — Inspect  ion. ^Thia  affords  but  little  if  any 
information,  owing  to  the  fact  that  in  most  eases  distention  of  the 
chest  has  already  been  produced  by  associated  hydrothorax  or  the 
heart  and  lungs  have  been  crowded  ujiward  by  ascites.  Should 
some  local  disease  have  occasioncul  the  hydropericardium,  and  the 
thoracic  ])arietes  l)e  sniiicieiit  ly  yieldiui:,  tliei-e  will  be  more  or  less 
I)ra'Cordial  bulging,  togetlier  with  absence  of  cardiac  impulse. 

Paljmlioii. — Wluit  has  been  said  regarding  inspection  applies 
also  to  palpation.  The  chief,  and  perhaps  the  only  thing  noted,  i? 
absence  of  cardutc  impulse,  and  possibly  a  sense  of  increased  prai- 


HYDROPERICARDIUM  129 

cordial  resistance.  The  pulse  presents  nothing  characteristic, 
since  the  changes  observed  in  it  are  also  produced  by  the  primary 
cardiac  affection. 

Percussion. — This  affords  us  our  chief  means  of  diagnosis,  the 
same  as  in  pericardial  effusion;  for  particulars  the  reader  is  re- 
ferred to  what  has  already  been  said  under  that  head.  Owing  to 
the  probable  association  of  hydropericardium  with  hydrothorax, 
the  characteristic  shape  of  praBcordial  dulness  is  likely  to  be  modi- 
fied by  and  merge  into  that  of  the  latter  affection.  Under  such 
circumstances,  it  would  only  be  at  the  upper  part  of  the  sternum 
that  percussion  might  be  of  any  special  value  as  regards  the  detec- 
tion of  the  hydropericardium.  If  the  area  of  cardiac  flatness 
extends  high  up  towards  the  suprasternal  notch,  with  a  bluntly 
rounded  apex,  well  above  the  area  of  dulness  due  to  the  hydro- 
thorax,  this  fact  might,  theoretically  at  least,  be  of  aid  in  deter- 
mining the  existence  of  transudation  into  the  pericardium. 

Auscultation. — Owing  to  the  intervention  of  fluid  between  the 
heart  and  the  chest-wall,  cardiac  sounds  are  feeble  and  distant,  and 
they  may  indeed  be  almost  inaudible.  If  murmurs,  due  to  some 
pre-existing  valvular  disease,  are  also  present,  these  are  likewise 
enfeebled. 

Diagnosis. — From  the  foregoing  considerations  it  is  evident 
that  the  diagnosis  of  hydro23ericardimn  is  not  only  difiicult,  but 
may  be  actually  impossible. 

In  those  extremely  rare  cases  of  pericardial  dropsy  due  to  local 
causes  the  diagnosis  is  governed  by  the  same  principles  as  in  mass- 
ive pericardial  exudation. 

The  differential  diagnosis  between  these  two  conditions  is  to 
be  made  by  the  history,  symptoms,  associated  diseases,  and  pres- 
ence or  absence  of  pericardial  friction.  In  effusion  there  is  his- 
tory of  rheumatism  or  some  acute  infectious  disease,  of  pyrexia, 
prsecordial  pain,  palpitation,  etc.  Even  in  distention  of  the  sac 
pericardial  friction-sounds  may  be  retained.  In  hydropericar- 
dium, on  the  other  hand,  there  is  history  or  evidence  of  some 
chronic  valvular  or  renal  disease,  and  all  symptoms  of  acute  in- 
flammation are  wanting,  and  there  is  no  pericardial  rub. 

Prognosis. — This  is  unfavourable,  both  because  of  the  nature 
of  the  primary  disorder  to  which  the  hydropericardium  is  second- 
ary, and  because  the  distention  of  the  sac  is  likely  to  hasten  car- 


130  DISEASES  OF  THE  HEART 

diac  failure.     The  prognosis  is  also  influenced  by  the  amenability 
to  treatment  of  the  cause  of  the  dropsy. 

Treatment. — This  resolves  itself  essentially  into  the  treat- 
ment of  the  primary  disorder,  since  with  the  removal  of  the  gen- 
eral dropsy  the  fluid  within  the  pericardium  is  absorbed.  Unless 
the  symptoms  be  exceedingly  threatening,  surgical  treatment,  if 
not  actually  unwise,  affords  only  a  very  temporary  relief.  In 
other  words,  the  treatment  of  hydropericardium  is  unavailing  un- 
less its  cause  can  be  remoyed.  The  management  of  dropsy  when 
associated  with  chronic  cardiac  disease,  will  be  found  fully  nar- 
rated in  subsequent  chapters. 

II.    n^MOPERICARDIUM 

By  this  term  is  not  meant  hai'morrhagic  pericarditis,  but  an 
extravasation  of  blood  into  the  pericardium  independent  of  any 
inflammatory  process.  It  is  fortunately  a  rather  rare  condition, 
and  yet  occurs  many  more  times  than  it  is  recognised.  It  requires 
but  very  brief  consideration. 

Morbid  Anatomy. — As  with  serous  transudation  or  effu- 
sion, the  escape  of  blood  into  the  pericardium  causes  a  distention 
of  the  sac  proportionate  to  the  amount  of  the  extravasated  blood. 
If  the  fia^morrhage  takes  place  rapidly  the  amount  discovered  post 
mortem  is  usually  not  large,  because  it  has  speedily  occasioned  the 
death  of  the  patient.  If,  on  the  other  hand,  it  takes  place  slowly, 
the  sac  may  be  greatly  distended.  The  blood  may  be  wholly  fluid 
or  have  undergone  more  or  less  coagulation.  After  the  evacuation 
of  the  pericardial  contents,  careful  scrutiny  discovers  evidence  of 
some  one  of  the  causes  of  the  haemorrhage. 

Etiology. — Blood  may  be  effused  into  the  pericardium  in 
consc(pience  of  external  injury,  as  by  gunshot  or  stab  wounds, 
laceration  of  the  sac  by  the  sharp  edge  of  a  fractured  rib,  etc.  It 
also  follows  rupture  of  the  heart-muscle,  the  bursting  of  an  aortic 
aneurysm,  or  in  rare  instances,  of  one  of  the  coronary  arteries.  It 
is  stated  that  sacculated  aneurysms  of  the  ascending  arch  fre 
quently  rupture  into  the  pericardium.  Of  953  cases  of  aortic 
aneurysm  analyzed  by  Hare  and  Holder,  death  took  place  from 
rupture  289  times,  and  of  these,  75  cases  ru]itured  into  the  peri- 
cardium. Rupture  of  the  heart  occurs  from  degeneration  of  the 
myocardium,  and  is  fortunately  a  comparatively  infrequent  event. 


H^MOPERICARDIUM  131 

Laceration  of  the  heart-wall  has  occasionally  been  observed  to  fol- 
low a  crushing  injury  to  the  chest. 

Symptoms. — As  would  naturally  be  expected,  hicmorrhage 
into  the  pericardial  sac  occasions  the  very  gravest  symptoms.  If 
this  takes  place  slowly  through  a  minute  slip  in  the  wall  of  the 
heart  or  aorta,  symptoms  come  on  gradually,  and  are  those  of  acute 
aniTcmia,  together  with  slowly  induced  and  progressive  heart-fail- 
ure. These  are  a  sense  of  precordial  distress,  anxiety,  weakness 
and  prostration,  dyspnoea,  pallor  with  cyanosis,  a  weak,  rapid, 
perhaps  irregular,  pulse,  coldness  of  the  extremities,  and  clammy 
perspiration.  Death  takes  place  within  a  few  hours,  or  perhaps  a 
day  or  two. 

Should  the  haemorrhage  be  free,  and  the  sac  become  rapidly 
distended,  the  symptoms  are  those  of  sudden  and  profound  shock, 
the  patient  passing  quickly  into  a  state  of  collapse,  and  dying  in 
a  few  minutes.  If  the  rupture  does  not  occasion  appreciable  pain 
there  may  be  nothing  in  the  symptoms  to  direct  attention  to  the 
pericardium.  In  most  instances  the  course  is  rapid,  leading  to  a 
speedily  fatal  termination. 

Physical  Signs. — These  are  the  signs  of  fluid  distention  of 
the  sac,  and  hence  do  not  require  repetition.  In  the  majority  of 
instances  death  is  too  rapidly  induced  or  the  distention  of  the 
pericardium  too  small  to  occasion  appreciable  physical  signs. 

Diagnosis. — If  the  life  of  the  patient  is  sufficiently  prolonged, 
and  if  the  sac  is  sufficiently  filled,  it  is  possible  for  the  trije  nature 
of  the  difficulty  to  be  recognised  by  examination  of  the  prsecor- 
dium.  If  the  presence  of  fluid  in  the  pericardium  is  made  out,  the 
history  of  its  sudden  appearance  and  the  symptoms  of  shock  and 
collapse  will  probably  enable  one  to  surmise  at  least  the  true  na- 
ture of  the  malady  and  to  differentiate  it  from  hydropericardium. 
Diagnosis  may  also  be  facilitated  by  history  of  some  antecedent 
affection  as  aneurysm,  likely  to  lead  to  haemorrhage. 

Prognosis. — If  ha^mopericardium  results  from  trauma,  the 
prognosis  depends  upon  whether  or  not  the  injury  is  amenable  to 
surgical  treatment.  In  cases  due  to  aortic  or  cardiac  rupture  the 
prognosis  is  absolutely  unfavourable,  and  death  is  the  inevitable, 
it  may  be  the  immediate,  result. 

Treatment. — This  in  traumatic  cases  is  surgical,  and  is 
best  left  to  text-books  on  surgery.    In  the  other  class  of  cases  there 


132  DISEASES  OP  THE  HEART 

is  no  treatinciit,  oxce]it  possiblv  in  those  raro  instanco.=!  of  trau- 
matic laceration  of  the  lieart,  when  the  surgeon  should  promptly 
lay  open  the  sac,  evaeutc  the  hlood,  in  the  hope  of  discovering  the 
source  of  the  luemorrliage,  and  of  being  able  to  repair  the  injury 
by  suturing  the  heart-muscle. 

Medicinal  treatment  is  limited  to  stimulation  of  the  heart 
and  an  attempt  to  support  the  powers  of  life.  In  most  instances 
the  physician  arrives  on  the  scene  too  late  to  do  more  than  witness 
the  death-struggle  or  sign  the  death-certificate. 

III.    PNEUMOPERICARDIUM 

This  is  so  extremely  rare  an  affection  that  but  few  have  been 
so  fortunate  as  to  observe  an  instance  of  the  kind.  By  this  term 
is  meant  a  collection  of  air  or  gas  within  the  pericardial  sac,  and 
hence  it  is  the  counterpart  of  the  condition  known  as  pneumo- 
thorax. 

Morbid  Anatomy. — Pneumopericardium  is  usually  associ- 
ated with  collection  of  fluid,  most  commonly  of  pus,  wdthin  the 
sac.  The  amount  of  contained  air  or  gas  is  variable,  but  is  sufii- 
cient,  together  with  the  exudation,  to  occasion  great  distention. 
If  the  gas  is  not  absorbed,  and  the  pericardium  be  opened  post 
mortem,  the  gas  escapes  with  a  hissing  noise  and  often  possesses 
a  fd'tid  odour.  In  some  instances  its  avenue  of  entrance  can  be 
easily  ascertained,  while  in  others  there  is  no  discoverable  open- 
ing into  the  pericardium,  either  because,  if  such  have  existed, 
it  has  become  closed,  or  because  the  gas  has  been  generated 
in  loco.  There  are  usually  present  also  evidences  of  acute  peri- 
carditis. 

Etiology. — Pneumopericardium  may  be  produced  in  any  one 
of  tlirec  ways:  (1)  Perforation  of  the  sac  from  without  may 
allow  of  the  entrance  of  atmospheric  air;  (2)  communication 
may  be  established  between  the  sac  and  some  portion  of  tlie  digest- 
ive tract,  thus  permitting  the  ingress  of  the  gases  normally  exist- 
ing in  the  latter;  or  (3)  gas  may  be  generated  within  the  peri- 
cardium without  solution  of  its  continuity.  The  entrance  of 
atmospheric  :iir  into  the  sac  usually  takes  place  through  a  ])erfo- 
rating  wound,  as  from  a  bullet  or  some  stabbing  instrument.  In 
rare  instances  air  may  enter  the  pericardium  thi'ough  tlie  lung  in 
consequence  of  laceration  l)y  the  shai-p  edge  of  the  fractured  star- 


PNEUMOPERICARDIUM  133 

nnm  or  rib,  or  by  rupture  of  a  pulmonary  cavity  situated  in  im- 
mediate contiguity  to  the  sac. 

When  a  communication  is  established  between  the  pericardium 
and  oesoj)hagus,  air  is  forced  into  the  former  with  each  act  of  swal- 
lowing. Walshe  has  narrated  an  interesting  case  of  perforation 
of  the  pericardium,  and  resulting  pneumopericardium,  during  an 
attempt  by  a  juggler  to  swallow  a  short  sword. 

When  gas  is  admitted  to  the  sac  from  some  one  of  the  hollow 
viscera  it  is  usually  in  consequence  of  the  extension  of  a  previ- 
ously existing  ulcerative  process.  The  most  frequent  communi- 
cation formed  in  this  way  is  with  the  stomach,  by  reason  of  an 
ulcer,  when  situated  on  its  posterior  wall.  Of  28  cases  of  perfora- 
tion of  the  diaphragm  by  gastric  ulcers  collected  by  Ludwig  Pick, 
only  10  were  cases  in  which  the  ulceration  had  perforated  the 
pericardium.  CoUingwood  Fenwick  records  a  very  interesting- 
case  which  occurred  in  his  practice,  in  which  a  gastric  ulcer  had 
perforated  the  pericardium  with  an  immediately  fatal  result,  and 
yet  no  previous  symptoms  had  occurred  to  point  to  the  presence 
of  the  gastric  ulcer.  In  4  of  the  10  cases  collected  by  Pick  the 
two  surfaces  of  the  pericardium  had  become  adherent  before  the 
ulceration  had  perforated,  so  that  the  ulcerative  process  involved 
the  substance  of  the  heart  itself.  Ulceration  into  the  sac  may 
also  take  place  from  the  oesophagus,  but,  as  already  stated,  atmos- 
pheric air  is  then  admitted,  instead  of  stomach  or  intestinal  gases. 

In  the  minds  of  some,  the  spontaneous  development  of  pneumo- 
pericardium is  a  matter  of  doubt.  Gibson  is  of  the  opinion  that 
in  some  of  the  cases  supposed  to  be  of  this  origin  the  pneumoperi- 
cardium was  in  reality  the  result  of  an  opening  into  the  sac, 
which,  however,  became  so  quickly  and  perfectly  closed  that  no 
trace  of  such  opening  could  be  discovered.  IsTevertheless,  the 
discovery  of  gas-forming  bacilli  renders  intelligible  and  possible 
the  spontaneous  development  of  pneumopericardium,  and  may  ex- 
plain some  cases  that  would  be  difficult  or  impossible  to  account 
for  on  any  other  hypothesis.  This  mode  of  production  is  exceed- 
ingly infrequent,  to  say  the  least.  Such  a  pneumopericardium  is 
preceded  or  accompanied  by  acute  suppurative  or  hsemorrhagic 
pericarditis. 

Symptoms.- — Subjective  manifestations  are  essentially  those 
of  sudden  distention  of  the  sac  from  any  other  cause.     They  are 


134:  DISEASES  OF  THE   HEART 

symptoms  of  pressure ;  but  inasmuch  as  the  entrance  of  gas  takes 
place  suddenly,  symptoms  develop  rapidly  and  are  extreme.  In 
some  instances  there  are  symptoms  of  shock;  a  weak,  irregular 
pulse,  a  pale,  anxious  countenance,  the  skin  covered  with  cold 
sweat,  which,  together  with  orthopnooa,  produces  a  picture  of  mor- 
tal agony.  The  physician's  attention  is  at  once  directed  to  the 
heart,  the  examination  of  which  reveals  a  most  singular  group  of 
objective  symptoms. 

Physical  Signs.- — Insijection  and  Palpation. — These  afford 
evidence  of  pericardial  distention  but  not  of  the  .nature  of  the  dis- 
ease, and  are  of  minor  importance  since  the  diagnosis  is  readily 
established  by  other  means  of  exploration  at  our  disposal. 

Percussion. — The  phenomena  perceived  by  percussion  are 
unique ;  instead  of  cardiac  dulness,  encroached  upon  and  sur- 
rounded by  pulmonary  resonance,  the  pra?cordiuni  is  found  to  be 
tympanitic,  either  throughout  or  at  its  upper  portion.  If  the  peri- 
cardium contains  fluid,  as  well  as  air  or  gas,  there  is  dulness  over 
the  dependent  part  and  high-pitched  tympany  above.  Gas  being 
lighter  than  the  exudate,  change  in  the  patient's  position  from  the 
recumbent  to  the  upright,  and  from  side  to  side,  causes  the  gas 
to  move  about,  so  as  to  be  always  above  the  level  of  the  fluid; 
hence  there  is  change  in  the  location  of  dulness  and  tympany  ac- 
cording to  the  posture  of  the  i)atient.  In  the  erect  position  dul- 
ness occupies  the  bottom  and  tympany  the  apex  of  the  sac.  If  the 
patient  lies  on  his  left  side  the  fluid  gravitates  in  that  direction, 
with  corresponding  dulness  surmounted  by  tympany ;  and,  on  the 
other  hand,  the  assumption  of  the  right  lateral  decubitus  causes  a 
corresponding  alteration  in  the  relative  position  of  the  gas  and 
liquid,  with  resulting  transposition  of  tympany  and  dulness. 
Moreover,  the  larger  the  amount  of  exudate  the  smaller  the  space 
allotted  to  the  gas,  and  hence  the  higher  the  pitch  of  the  tym- 
panitic note.  Stokes  claimed  in  one  case  to  have  detected 
"  cracked-pot "  resonance. 

AuscuUation. — Perhaps  the  most  striking  features  are  the 
peculiar  sounds  ol)served  on  auscultation.  The  movements  of  the 
heart  cause  an  agitation  of  the  gas  and  li(|uid  contents  of  the  sac, 
and  hence  a  true  succussion-sound  or  splaslhin.g.  This  is  variously 
described  as  churning,  splashing,  or  like  that  produced  by  a  water- 
wheel.     These  are  sometimes  accompanied  by  that  musical  sound 


PNEUMOPERICARDIUM  135 

known  as  the  metallic  tinkle,  likened  to  the  dropping  of  water. 
This  pericardial  splashing  is  of  precisely  the  same  character  as  the 
hypocratic  succussion-sound  elicited  by  shaking  a  patient  with 
pneumohydrothorax.  In  some  instances  these  metallic  sounds  are 
audible  at  a  distance  from  the  patient's  chest. 

Diagnosis. — This  combination  of  a  clear  ringing  tympanitic 
percussion-note  with  sjDlashing  in  the  cardiac  area  is  so  unique 
that  an  erroneous  diagnosis  can  scarcely  be  made.  It  seems  to  me, 
therefore,  far  afield  to  discuss  the  differential  diagnosis  between 
this  affection  and  dilatation  of  the  stomach  or  pulmonary  vomica 
in  immediate  proximity  to  the  heart,  which  are  conditions  said  by 
some  authors  to  render  a  mistake  in  diagnosis  possible.  Finally, 
the  confounding  of  this  disease  with  the  presence  of  air  and  fluid 
within  the  pleural  cavity  is  scarcely  likely,  if  one  will  bear  in 
mind  that  in  pneumothorax  the  succussion-sound  is  only  obtained 
when  the  patient's  body  is  agitated,  while  in  the  affection  under 
discussion  the  peculiar  sound  is  present  even  when  the  patient  is 
at  rest. 

Prognosis. — This  is  always  serious,  yet  in  traumatic  cases 
there  is  hope  of  cure  through  surgical  interference,  while  the  same 
may  be  said  regarding  cases  associated  with  purulent  pericarditis. 
Should  gas  gain  entrance  to  the  pericardium,  and  be  not  followed 
by  infection  of  the  sac  and  inflammation,  there  is  a  possibility  of 
its  ultimate  absorption.  Moreover,  the  prognosis  depends  upon 
the  suddenness  of  the  formation  of  pneumopericardium.  If  this 
is  sufficiently  rapid  to  occasion  symptoms  of  shock,  there  is  strong 
likelihood  that  the  patient  will  succumb.  If,  on  the  other  hand, 
the  condition  develops  slowly,  symptoms  may  not  be  very  urgent, 
and  time  may  be  allowed  for  surgical  intervention. 

Treatment. — It  goes  without  saying,  that  in  most  cases  if  sur- 
gical skill  cannot  remove  the  cause,  other  treatment,  no  matter  how 
energetic,  will  be  found  unavailing.  The  same  principles  govern 
the  therapeutic  management  as  in  other  forms  of  pericardial  dis- 
ease. Supporting  and  stimulating  measures  are  aways  indicated, 
and  may  even  enable  the  patient  to  rally  from  the  initial  shock. 
Pain  and  distress  should  be  relieved  by  a  dose  of  morphine  admin- 
istered hypodermically.  Heat  should  be  applied  to  the  extremi- 
ties. Camphor,  ammonia,  ether,  and  brandy  are  useful  stimu- 
lants, and  should  be  given  freely.     The  physician  should  not  for- 


13G  DISEASES  OP  THE   HEART 

get  the  great  value  of  stryeliniue  and  digitalis  in  su])])ortiiig  the 
heart;  the  former  should  be  administered  under  the  skin. 

IV.    TUBEK(  TLOSIS   OF   THE   PEKICAKDIUM 

Morbid  Anatomy. — Tuberculosis  produces  in  the  pericar- 
dium all  of  the  characteristic  lesions  to  which  it  may  give  rise  in 
other  regions  of  the  body.  The  process  may  be  acute  or  chronic 
in  course,  and  either  exudative,  productive,  or  destructive  in 
nature. 

The  acute  process  is  not  often  to  be  distinguished  from  an 
ordinary  acute  pericarditis  except  by  microscopic  and  bacterio- 
logical methods.  The  exudate  may  be  fibrinous,  sero-fibrinous,  or 
jnirulent,  but  tuberculous  pericarditis  shares  with  the  inflamma- 
tion of  malignant  disease  the  distinction  of  being  the  most  fre- 
quent cause  of  lux'morrliagic  exudation  in  the  pericardium.  Tuber- 
cles may  not  be  demonstrable  post  mortem,  and  when  found  are 
often  exceedingly  small,  even  microscopic.  They  are  usually 
found  on  the  parietal  layer  of  the  sac,  owing  to  the  frequency  with 
which  the  infection  extends  from  neighbouring  viscera.  The  mil- 
iary tubercles  may  be  covered  by  the  fibrinous  exudate,  and  are 
then  to  be  discovered  by  detaching  tlu;  fibrin.  They  uuiv,  however, 
be  easily  seen,  and  when  collected  in  groups  give  rise  to  areas  of 
caseation.  These  caseous  areas  may  invade  the  myocardium,  and 
in  one  instance  a  cheesy  mass  had  perforated  the  wall  of  an  auri- 
cle and  projected  into  its  cavity,  being  covered  by  a  thrombus 
where  it  was  in  contact  with  the  blood. 

Again,  when  the  production  of  granulation  tissue  is  the  pre- 
dominating feature  of  the  ])rocess,  the  two  layers  of  the  pericar- 
dium are  bound  together  by  a  bluish  translucent  mass  of  new- 
formed  tissue.  This  of  course  becomes  white  as  it  grows  older, 
and  the  condition  of  adherent  pericardiimi  is  produced.  Only 
rarely  is  the  caseous  mass  calcified  after  the  cessation  of  the  active 
process — calcification  being  more  comiiioii  in  the  inspissated  re- 
mains of  })urulent  exudates. 

Acute  pericarditis  is  probaI)ly  tuberculous  in  a  larger  propor- 
tion of  cases  than  has  been  supposed,  and  indeed  cannot  be  con- 
sidered a  rare  condition.  Of  1,048  autospies  on  adults  dead  from 
all  eauses,  Wells  found  this  condition  in  10  cases,  or  nearly  1  per 
cent;  and  since  in  128  cases  the  pericardium  was  actively  involved, 


TUBERCULOSIS  OP  THE  PERICARDIUM  137 

the  10  cases  ainoiint  to  about  8  per  cent.  Osier  reports  7  per  cent 
from  his  series  of  cases. 

Chronic  tuberculous  pericarditis  may  follow  an  acute  attack, 
and  in  this  case  the  post-mortem  findings  are  those  of  an  ordinary 
chronic  j)ericarditis,  with  the  addition  at  times  of  grayish  tuber- 
cles, or  of  areas  undergoing  caseous  degeneration.  It  is  the  excep- 
tion, however,  rather  than  the  rule,  to  find  distinct  evidences  of 
tuberculous  origin,  even  in  cases  in  which  the  clinical  history 
almost  conclusively  proves  this.  Indeed,  in  spite  of  the  large 
number  of  cases  of  acute  pericarditis  that  are  tubercular,  and 
which  pass  on  into  the  chronic  form,  it  is  very  exceptional  to  dis- 
cover any  conclusive  post-mortem  evidence  of  tuberculosis  in  cases 
of  chronic  pericarditis.  The  findings  include  thickening  of  the 
membrane  and  more  or  less  complete  adhesions  of  the  two  layers, 
the  translucent  bluish  granulation  tissue  of  the  acute  stage  having 
been  replaced  by  firm,  white  cicatricial  tissue. 

Pericardial  tuberculosis  may  be  chronic  from  the  outset,  in 
which  event  the  lesions  are  more  apt  to  be  of  a  distinctly  tuber- 
culous nature,  tubercles  and  caseating  areas  being  common. 

Etiology. — Authors  distinguish  a  primary  as  well  as  a  sec- 
ondary form  of  pericardial  tuberculosis.  According  to  Osier,  the 
primary  form  may  be  "  associated  only  with  caseation  of  the  bron- 
chial or,  ^particularly,  the  anterior  mediastinal  glands."  In  other 
cases  there  are  no  such  associated  lesions,  and  in  these  the  tuber- 
culous affection  of  the  pericardium  is  mipossible  to  explain. 

The  secondary  form  is  the  one  generally  encountered,  and  de- 
pends upon  previously  existing  tuberculous  disease  elsewhere  in 
the  body.  This  may  be  caries  of  a  vertebra,  a  rib,  or  the  sternum, 
caseous  bronchial  or  mediastinal  glands,  tuberculosis  of  the  lung, 
pleura,  or  retroperitoneal  lymph-glands,  or  tuberculous  peritonitis. 
Occasionally  miliary  tubercles  within  the  pericardium  are  a  part 
of  a  general  miliary  infection. 

This  form  of  pericardial  disease  is  most  common  between  the 
ages  of  fifteen  and  thirty,  yet  has  been  seen  in  individuals  at  either 
extreme  of  life.  Osier  met  with  a  case  in  a  child  of  five,  Duck- 
worth in  an  infant  of  only  five  months,  and  Lajard  in  a  woman 
of  eighty-eight.  A  patient  of  mine  who  died  of  pulmonary  con- 
sumption, with  acquired  dextrocardia,  and  in  whose  adherent 
pericardium  tubercles  existed,  was  a  j'Oung  man  of  eighteen.  The 
11 

/ 


138  DISEASES  OP  THE  HEART 

disease  affects  both  sexes,  but  for  some  strange  reason  appears  to 
be  rather  more  common  in  males.  Other  predisposing  causes  are 
all  those  conditions  that  render  an  individual  susceptible  to  this 
form  of  infection. 

Symptoms. — In  most  cases  the  disease  is  wholly  latent,  and  is 
only  discovered  on  the  autopsy  table.  This  is  due  to  the  fact  that 
the  disease  is  generally  subacute  or  chronic,  and  arises  insidiously. 
If  it  gives  rise  to  ac\ite  inflammation  with  effusion  the  symptoms 
arc  those  of  acute  pericarditis  from  other  causes — pain,  palpita- 
tion, fever,  friction-sounds,  and,  upon  distention  of  the  sac,  the 
pressure-effects  already  considered.  Even  an  exudative  pericar- 
ditis of  this  origin  nuiy  in  some  instances  pursue  a  chronic  course. 

Physical  Signs. — Objective  manifestations  of  the  disease 
are  wanting  unless  the  affection  is  declared  as  an  acute  process. 
When  such  is  the  case  there  are  the  fremitus,  pericardial  friction- 
sound,  and,  with  filling  of  the  sac  by  exudation,  the  evidence  of 
fluid  distention — i.  e.,  triangular  area  of  dulness  and  disappear- 
ance of  the  cardiac  impulse,  etc. ;  in  short,  the  signs  already  de- 
scribed in  the  chapter  on  Acute  Pericarditis. 

Diagnosis. — Owing  to  the  insidious  onset  and  latent  naturb 
of  this  disease  it  is  rarely  diagnosticated  during  life.  If  in  the 
course  of  pulmonary  tuberculosis  or  of  pleuritis  in  a  tuberculous 
subject  the  physical  signs  of  pericardial  involvement  should  make 
their  appearance,  one  might  with  confidence  make  the  diagnosis 
of  pericardial  tuberculosis ;  but  without  such  favouring  conditions 
it  is  not  at  all  likely  that  the  disease  would  be  discovered. 

Prognosis. — This  is  not  always  serious  so  far  as  it  affects 
the  duration  of  life,  yet  it  undoubtedly  contributes  its  share  to 
the  unfavourable  termination  of  the  general  tuberculous  disease. 
Its  remote  effects  are  an  adherent  pericardium  and  cardiac  insuffi- 
ciency. The  appearance  of  a  tuberculous  pericardial  effusion  in 
the  late  stages  of  pulmonary  tuberculosis,  the  patient  being  al- 
ready rnflu'C'tio,  would  undoubtedly  hasten  the  fatal  issue. 

Treatment. — This  is  to  be  conducted  on  the  lines  already  laid 
down  for  the  management  of  other  forms  of  acute  pericarditis. 

V.   SYPHILIS  OF  THE   PERICARDIUM 

Invasion  of  the  pericardium  by  sy])liilis  is  so  rare  an  affection 
that  most  text-books  on  diseases  of  tlic  Iicnrt   citlier  do  not  con- 


SYPHILIS  OF  THE  PERICARDIUM  139 

sider  it  at  all  or  give  it  the  very  briefest  possible  mention.  Eich- 
horst,  for  example,  simply  states  that  gaimmata  in  this  situation 
have  been  described  by  Lancereaux  and  Orth.  In  Allbutt's  Sys- 
tem of  Medicine  I  fail  to  find  any  mention  of  syphilis  under  dis- 
eases of  the  pericardium,  and  the  same  may  be  said  of  Hayden 
,  and  Walslie  in  their  classical  works  on  the  heart.  Gibson,  whose 
remarks  on  this  subject  are  more  voluminous,  devotes  but  a  single 
page  to  it,  and  would  seem  to  have  been  largely  indebted  to  Mra- 
cek's  jDaper,  which  has  likewise  furnished  the  inspiration  for  the 
following  brief  consideration: 

Morbid  Anatomy. — Syphilis  of  the  pericardium  is  always 
a  very  rare  affection,  and  is  almost  never  met  with  unassociated 
with  syphilitic  changes  in  the  heart-muscle.  When  present,  the 
disease  is  limited  to  the  visceral  layer  and  manifests  itself  either 
as  gummata  or  circumscribed  thickenings.  Although  cases  have 
been  described  as  syphilitic  pericarditis  with  sero-fibrinous  exu- 
dation, Mracek  is  of  the  opinion  that  their  syphilitic  nature  is 
open  to  doubt.  Of  the  two  forms  in  which  pericardial  syphilis 
declares  itself,  fibrinous  thickening  is  much  the  more  common. 
At  the  time  Mracek's  monograph  appeared  only  3  authenticated 
cases  of  gumma  within  the  pericardium  had  been  described — one 
each  by  Lancereaux,  Orth,  and  Mracek. 

The  portions  of  the  epicardium  that  appear  thickened  and 
fibrous  are  usually  found  to  overlie  and  be  intimately  connected 
with  areas  of  proi;ounced  myocardial  fibrosis  or  a  gumma  situated 
within  the  heart-muscle.  The  development  of  connective  tissue 
usually  begins  in  the  immediate  neighbourhood  of  the  blood-ves- 
sels, and  then  extends  more  or  less  widely  into  the  surrounding 
parts. 

In  the  second  case  of  Mracek's  series,  in  which  the  epicardium 
was  thickened  and  elevated  in  a  circumscribed  zone,  immediately 
overlying  a  small  gumma,  the  microscope  revealed  signs  of  recent 
inflammation  of  the  adipose  tissue.  This  tissue  was  thickly  infil- 
trated with  cells,  particularly  in  those  parts  next  to  the  muscle- 
substance  and  around  the  borders  of  the  gummy  tumour.  Imme- 
diately above  the  gumma  there  was,  in  addition  to  cellular  infiltra- 
tion, a  pronounced  hyperaemia  of  the  veins  and  capillaries.  On 
the  overlying  surface  of  the  epicardium  the  fibrous  tissue  was  old 
and  firm. 


140  DISEASES  OF   THE   HEART 

In  the  course  of  time  the  blood-vessels  suppl^'ing  the  newly 
formed  connective  tissue  undergo  obliteration,  and  the  latter  be- 
comes transformed  into  firm  cicatricial  tissue.  Thickening  of  the 
serous  membrane  is  not  necessarily  associated  with  a  deposit  of 
fibrin,  and  consequently  pericardial  adhesions  are  not  always  ob- 
served. In  some  instances,  however,  the  two  layers  are  found 
loosely  united  in  the  areas  in  which  the  connective  tissue  has 
undergone  hyperplasia.  Total  obliteration  of  the  sac  is  almost 
never  encountered. 

Syphilitic  pericarditis  is  a  very  chronic  process,  much  more 
so  than  is  tuberculous  pericarditis;  and  Mracek  affirms  that  in 
those  cases  in  which  it  is  difficult  to  determine  whether  the  process 
is  tuberculous  or  syphilitic,  the  presence  of  a  sero-fibrinous  or 
ha?morrhagic  exudation  tells  in  favour  of  its  tuberculous  origin. 
In  cases  of  exudative  pericarditis  syphilis  is  the  last  thing  to  be 
thought  of.  In  some  instances  the  sac  may  be  found  to  contain  a 
small  amount  of  clear  serum,  but  when  present  this  is  a  transuda- 
tion due  to  compression  of  the  blood-vessels  by  the  products  of 
sy})liilitic  disease.  Very  rarely  lupmopericardium  may  also  be 
produced,  as  in  one  case  by  a  rupture  of  a  small  cardiac  aneurysm, 
itself  the  result  of  syphilitic  fibrous  myocarditis. 

Etiology. — Syphilitic  disease  in  this  situation  is  a  late  mani- 
festation of  the  infection.  There  are  no  known  factors  which 
determine  its  invasion  of  the  pericardial  sac,  but,  as  it  is  a  consti- 
tutional disease,  it  is  only  singular  that  it  is  not  more  frequently 
2)resent  in  this  location. 

Symptoms. — Syphilis  of  the  pericardium  either  occasions 
no  syinj)tiiiiis,  or  these  arc  obscured  by  those  of  syphilitic  disease 
in  other  ])arts  of  tlie  body  or  in  tlie  heart-muscle.  luasniucli  as 
pericardial  clianges  of  this  nature  are  almost  always  found  in  con- 
nection with  luetic  disease  of  the  myocardium  or  endocardium,  it 
is  impossible  to  say  how  much,  if  any,  of  the  symptomatology  is  to 
be  attributed  to  the  pericardial  disease.  It  is  liighly  probable, 
however,  that  the  chief  role  in  this  res])ect  is  ])layed  by  the  myo- 
cardial (h'geueration  or  the  sclerotic  endocarditis,  as  the  case  may 
be.  The  cardiac  niaiiifcstations  will  be  fully  described  in  the 
cliii|)tcr  on   Heart  Sy])liilis. 

Physical  Signs. — l^lx<'c|)t  in  the  rare  cases  in  which  the 
pericardial  changes  lead   to  tli(;  development  of  a  friction-sound 


CARCINOMA  AND  SARCOMA   OP  THE   PERICARDIUM        141 

or  to  dropsical  distention  of  the  sac,  there  are  no  distinctive  ob- 
jective signs  of  the  local  disease. 

Diagnosis. — Even  in  a  luetic  patient  with  distinct  cardiac 
symiDtoms,  they  are  far  more  likely  to  be  due  to  syphilis  of  the 
myocardium  than  of  the  pericardium,  and  hence  one  should  be 
very  guarded  in  making  the  diagnosis  of  the  latter  condition.  The 
intra-vitam  recognition  of  pericardial  syphilis  is  on  the  whole, 
therefore,  very  unlikely. 

Prognosis. — Per  se  pericardial  syphilis  cannot  be  regarded 
as  a  dangerous  affection;  the  adhesions  it  induces  are  usually  so 
circumscribed  and  loose  that  they  probably  exert  little  if  any  in- 
jurious influence  in  the  way  of  cardiac  hypertrophy  and  dilata- 
tion. In  general  it  may  be  stated  that  the  prognosis  is  that  of 
syphilitic  disease  of  the  heart-muscle,  which,  as  experience  shows, 
is  very  amenable  to  proper  management. 

Treatment. — This  consists  of  the  vigorous  employment  of 
mercury  and  the  iodides,  and  need  not  here  be  discussed. 

VI.    CARCINOMA  AND   SARCOMA   OP  THE   PERICARDIUM 

Malignant  disease,  like  syphilis,  attacks  the  pericardium  with 
such  infrequency  as  to  merit  but  brief  consideration. 

Morbid  Anatomy. — Owing  to  the  extreme  rarity  of  pri- 
mary tumours  of  the  sac,  but  little  can  be  said  concerning  them. 
Williams  and  Miller  have  reported  a  case  of  sarcoma  of  the  peri- 
cardium in  a  boy  of  thirteen.  The  tumour  was  a  diffuse,  small- 
celled  sarcoma  of  the  parietal  layer,  which  had  produced  uniform 
thickening,  but  had  not  invaded  the  epicardium.  There  was  no  dis- 
coverable involvement  of  the  lymph-nodes  in  any  other  part  of  the 
body,  and  for  this  and  other  reasons  the  authors  concluded  that  the 
growth  had  originated  in  the  lymphatic  structures  of  the  sac  itself. 

Of  secondary  tumours,  those  most  commonly  invading  the  sac 
are  lymphosarcoma  from  the  mediastinal  nodes,  and  carcinoma 
from  the  stomach  or  oesophagus.  The  new  growth  may  uniformly 
infiltrate  the  parietal  layer  of  the  sac,  or  single  nodules  may  pro- 
ject into  its  interior.  There  is  always  more  or  less  fluid  in  the 
sac,  either  of  inflammatory  or  of  dropsical  nature.  The  inflam- 
mation due  to  cancerous  disease  of  the  pericardium  is  particularly 
apt  to  produce  a  ha?morrhagic  exudate — being  in  this  regard  like 
the  tuberculous  disease. 


142  DISEASES  OF  THE  HEART 

Etiology. — Primary  malignant  disease  of  the  pericardium  is 
so  rare  that,  according  to  Gibson,  the  only  authentic  case  on  record 
was  the  one  observed  by  Koester.  Sir  William  Broadbent  has, 
however,  reported  an  instance  of  sarcoma,  which  was  thought  to 
be  primary,  and  I  have  mentioned  above  the  case  reported  by 
Williams  and  Miller.  In  the  vast  majority  of  cases  this  affection 
of  the  sac  is  secondary  to  new  growths  in  other  situations,  as  in 
the  (psopliagus,  lungs,  pleura,  mediastinal  glands,  liver,  etc. 

Symptoms. — As  a  rule  this  disease  of  the  pericardium  is 
latent  or  the  clinical  picture  is  that  of  the  primary  tumour. 

Physical  Signs. — So  far  as  known,  there  are  no  distinctive 
physical  signs  of  malignant  invasion  of  the  pericardium.  If  such 
are  produced,  they  are  those  of  secondary  inflammation  or  of  drop- 
sical distention  of  the  sac,  and  require  no  repetition. 

Diagnosis. — This  is  rarely  if  ever  possible,  and  would  natu- 
rally depend  on  objective  manifestations  of  pericardial  disease, 
which,  as  just  stated,  are  very  uncertain. 

Prognosis  and  Treatment. — The  former  is  hopeless,  since 
the  disease  is  not  amenable  to  surgical  interference,  and  the  lat- 
ter must  be  confined  to  measures  calculated  to  relieve  suffering 
and  promote  euthanasia. 


SECTION  II 
DISEASES   OF  THE   ENDOOAEDIUM 


CHAPTEE   IV 

ACUTE    ENDOCARDITIS 

This  is  an  inflammation  of  the  lining  membrane  of  the  heart, 
which  it  has  long  been  customary  to  divide  into  two  forms,  for  rea- 
sons apparent  in  the  various  adjectives  applied  to  them.  Thus 
one  is  called  simple  or  benign,  because  it  does  not  often  destroy 
life  directly,  but  permits  the  patient  to  recover,  although  with 
valvular  lesion.  The  terms  vegetative  and  verrucose  are  also  ap-' 
plied  to  this  variety,  particularly  by  the  Germans,  on  account  of 
the  nature  of  the  inflammatory  changes  induced.  Simple  and 
benign  refer  to  its  clinical  manifestations,  verrucose  and  vegeta- 
tive to  its  anatomical  characters. 

The  other  form,  fortunately  much  less  frequent  than  the  pre- 
ceding, is  spoken  of  as  malignant,  to  designate  its  usually  fatal 
ending ;  and  infectious  or  infective,  in  allusion  to  certain  etiological 
and  clinical  characteristics.  Its  anatomical  features,  on  the  other 
hand,  are  shown  by  its  other  names — ulcerative,  dij^htheritic, 
mycotic.  Diphtheritic  was  applied  to  it  by  Virchow,  and  mycotic 
by  Winge,  who  was  the  first  to  describe  microbes  in  the  valves. 

In  conformity  with  the  plan  of  this  work,  which  is  to  desig- 
nate diseases  by  their  most  familiar  and  generally  employed 
names,  these  two  affections  will  be  spoken  of  as  acute  simple  and 
acute  ulcerative  endocarditis.  In  accordance  with  custom,  more- 
over, they  will  be  considered  as  distinct  clinical  entities,  although 
I  am  not  unmindful  of  the  fact  that  a  sharp  dividing  line  cannot 
always  be  drawn  between  them  either  clinically  or  anatomically. 

The  endocardium  may  become  inflamed  during  foetal  as  well 
as  extra-uterine  life;  but  the  two  halves  of  the  heart  are  affected 

143 


14-i  DISEASES  OF  THE   HEART 

with  different  degrees  of  frequency  during  these  two  periods  of 
existence.  After  birth  it  is  the  lining  membrane  of  the  left  side 
that  is  generally  attacked  by  inflammation,  as  is  so  well  shown  by 
Sperling's  oft-cited  statistics  of  300  cases  at  the  Berlin  Pathologi- 
cal Institute.  Of  these,  the  left  side  alone  was  found  affected  268 
times,  right  heart  alone  31  times,  both  together  29  times.  Of  the 
cases  affecting  the  left  side,  the  mitral  valves  were  involved  255 
times,  the  aortic  but  129  times. 

Morbid  Anatomy. — The  endocardium  is  the  lining  mem- 
brane of  the  heart,  and  is  continuous  with  the  intinia  of  the  blood- 
vessels through  the  various  openings  in  the  auricles  and  ventricles. 
It  consists  of  two  lamina:^ — a  fibrous,  very  thin  in  most  portions, 
and  an  endothelial,  the  latter  consisting  of  a  single  layer  of  flat- 
tened cells,  which  are  in  contact  with  the  blood. 

The  valves  of  the  heart  are  folds  of  the  endocardium,  the 
fibrous  layer  being  increased  to  give  them  greater  strength.  The 
valves  contain  no  muscular  tissue,  and  are  avascular,  with  excep- 
tion of  the  attached  margins  of  the  mitral  and  tricuspid  leaflets, 
which  contain  a  few  very  small  vessels.  These  are  the  only  por- 
tions of  the  endocardium  that  contain  blood-vessels,  as  the  mural 
endocardium,  as  well  as  the  remaining  portions  of  the  valves,  de- 
rives its  nutriment  from  the  blood  passing  over  it.  Lymphatics 
are,  however,  numerous. 

Anatomically,  it  is  exceedingly  difficult  to  draw  any  sharp  dis- 
tinction between  the  benign  and  malignant  forms,  as  all  inter- 
mediate grades  are  found  and  the  differences  seem  to  be  only  those 
of  intensity  of  the  process.  These  differences  are  doubtless  de- 
])endent  on  infection  by  different  organisms,  of  which  a  large  num- 
ber have  been  described  by  different  investigators. 

In  the  simple  form  the  first  change  visible  to  the  unaided  eye 
is  a  cloudiness  or  opacity  of  the  membrane.  This  is  probably  in 
all  cases  preceded  by  the  lodgment  of  micro-organisms  on  the  sur- 
face, which  had  been  rendered  vulnerable  by  some  previous  injury. 
Wyssokowitch,  Prudden,  and  others  have  shown  by  animal  experi- 
ments that  cultures  of  pathogenic  bacteria,  injected  into  the  cir- 
culation, })roduce  the  lesions  of  endocarditis  only  when  the  endo- 
cardium has  been  previously  injured,  as  by  passing  a  probe  doAvn 
the  carotid  artery  or  jugular  vein.  This  probably  explains  the 
fact  that  the  lesions  are  most  often  found  on  the  valvular  endoear- 


ACUTE   ENDOCARDITIS 


145 


(linm,  as  these  portions  are  most  liable  to  injury.  In  intra-uterine 
life  endocarditis  is  most  common  in  the  right  heart,  and  more 
often  on  the  tricuspid  than  on  the  pulmonary  valves. 

In  extra-uterine  life  the  lesions  are  most  common  on  the  mitral 
valve,  next  on  the  aortic,  and  only  very  rarely  on  the  valves  of 
the  right  side.     Furthermore,  the  lesions  are  usually  found,  not 


Fig.  24. — Verrucose  Endocarditis  of  Aortic  and  Mitral  Valves. 
Specimen  in  collection  of  Dr.  Gustav  Fiitterer. 


on  the  free  margins  of  the  valve-cusps,  but  along  a  line  correspond- 
ing to  the  point  of  maximum  contact  when  the  valves  close  (Fig. 
24).  In  the  case  of  the  auriculo-ventricular  valves  this  is  on  the 
auricular  surface,  while  on  the  semilunar  A^alves  it  is  on  the  ven- 
tricular surface.  From  these  facts  it  is  evident  that  the  work  that 
the  valve  has  to  do  and  the  strain  to  which  it  is  subjected  are  fac- 
tors in  the  determination  of  the  location  of  the  process. 


146 


DISEASES  OF   THE   HEART 


Following  the  appearance  of  cloudiness,  the  membrane  becomes 
thickened  and  adematoiis,  while  the  straining  and  pounding  to 
which  the  seg-ments  are  subjected  are  very  apt  to  produce  erosions 


ilP'li 


Fio.  25. — Verrucose  Endocarditis  of  Mitral  Valve. 
Specimen  in  collection  of  Dr.  Gustav  Fiitterer. 

or  lacerations.  These  naturally  occur  at  the  points  weakened  by 
the  invasion  of  micro-organisms,  and  if  tlu^  eroded  surface  is  not 
at  once  covered  l)y  the  deposit  of  tibiin  from  the  blood,  a  consid- 
erable loss  of  substance  may  take  place.  This  is  far  more  common, 
however,  in  the  malignant  form,  although  it  has  been  observed  in 
simple  endocarditis  comi)licating  rheunuitism.  !More  commonly 
the  eroded  surface,  necrotic  fi-om  the  action  of  bacteria,  is  at  once 
covered  by  a  de]X)sit  of  fibrin  from  the  blood.  This  fibrin  forms  a 
firm  warty  mass  of  a  yellowish  or  reddish  colour,  which  rises  above 
the  surface  of  the  membrane,  and  hence  has  received  the  name 


ACUTE   ENDOCARDITIS 


147 


of  vegetation.  The  name  is,  however,  not  very  appropriate,  as  the 
so-called  vegetation  is  in  its  formation  and  composition  a  throm- 
bus, and  may  contain  all  the  elements  of  a  thrombus,  fibrin,  red 
and  white  blood-corpuscles,  and  blood-platelets. 

By  the  time  that  the  vegetation  has  reached  such  a  size  as  to  be 
noticeable  to  the  unaided  eye,  the  process  of  repair  has  begun 
at  its  base.     'J'his  is  accomplished  by  the  ingrowth  of  young  con- 


FiG.  26. — Malignant  Vebbucose  Endocarditis  of  Mitral  VAL^•E. 
Specimen  in  collection  of  Dr.  Gustav  Fiitterer. 


nective-tissue  cells  and  the  formation  of  a  granulation  tissue 
which  finally  replaces  the  entire  mass  of  adherent  fibrin,  and  in 
time  becomes  covered  by  the  endothelium  from  the  neighbouring 


148  DISEASES   OF   THE    HEART 

mt'iiibraiie.  The  growth  can  now  he  more  i)ro])crly  terniod  a  vege- 
tation, as  it  is  essentially  an  outgrowth  from  the  snbjacent  tissue, 
and  some  authors  limit  the  term  to  this  form.  The  accumulation 
of  fibrin  over  such  an  afFeetcd  area  may  be  very  large,  but  the 
average  vegetation  is  about  8  millimetres  in  length.  When  of  the 
irregular  form  described,  the  endocarditis  is  spoken  of  as  the 
warty  or  verrucose  variety  (Figs.  24-27). 

The  vegetation  may  be  large  and  polypoid  in  shape  or  long 
and  string-like,  attached  at  one  end  so  as  to  swing  in  the  blood- 
stream. The  disease  is  then  spoken  of  as  of  the  polypoid  or  vil- 
lous variety  respectively.  The  vegetation  may  be  too  large  for 
complete  organization,  and  may  soften  and  redissolve  in  the 
blood-stream,  or  portions  may  break  off  and  be  carried  in  the 
blood  until  they  reach  a  vessel  of  too  small  calibre  to  permit  their 
passage,  when  they  plug  the  vessel  and  cut  off  the  circulation  of 
the  parts  sujjplied  by  it.  The  infarcts  thus  produced  by  the  emboli 
of  simple  endocarditis  are  usually  of  a  non-infective  nature. 

The  further  repaii-  of  these  lesions  and  the  changes  in  the 
valves  consequent  to  them  are  dealt  with  under  the  head  of 
Chronic  Endocarditis. 

The  malignant  form  of  the  disease  is  nuiinly  characterized  by 
the  intensity  of  the  infection,  and  the  fact  that  embolic  phenomena 
are  more  common  than  in  the  sim])le,  and  are  almost  always  of  a 
sei)tic  nature.  The  local  lesions  may  be  vegetative,  suppurative, 
or  ulcerative,  depending  on  the  nature  and  violence  of  the  infec- 
tion. In  all  cases  the  necrosis  of  the  affected  areas  is  more  marked 
than  in  the  simple  form,  and  ultimately  leads  to  loss  of  substance, 
the  portions  sloughed  off  passing  into  the  circulation  as  septic 
emboli. 

The  valve-cusp  thus  ulcerated  is  naturally  weakened,  and  fre- 
quently gives  way  before  the  pressure  of  the  blood,  forming  small 
pouches  in  the  valve,  the  so-called  vahuhii-  aneurysms,  or  giving 
way  completely  perforate  the  valves.  Acute  Viilvulai'  insufficiency 
can  thus  be  ])roduced  (Fig.  27).  A  valve-lea  lid  may  become 
partially  detached,  and  the  free  end  swing  in  the  blood-stream. 
Ulceration  of  the  ]i;i])illai-y  muscles  or  tlie  eliordie  tendina'  nuiy 
produce  stretching  or  I'ujjture  of  the  cords,  or  :i  tlii'()ud)us  covering 
the  affected  area  nuiy  mat  them  closely  together. 

When  the  lesions  are  situated  on  the  mural  endocardium,  per- 


ACUTE   ENDOCAKDITIS 


149 


foration  is  possible,  and  the  interventricular  sseptum  has  been 
found  perforated,  or  communication  has  been  established  between 
auricle  and  ventricle,  or  betAveen  the  right  auricle  and  the  aorta. 
When  the  disease  is  produced  bv  bacteria  of  suppuration,  abscess 


Tig.  27. — Malignant  Verrucose  Enducaeditis  of  Aortic  Valve,  with  Perforation 

OF  A  Cusp. 

Specimen  in  colleetion  of  Di'.  Gustav  Fiitterer. 


of  the  myocardium  may  result,  and,  discharging,  empty  its  con- 
tents into  the  circulation.     (Septic  Emboli.) 

Associated  with  acute  endocarditis  are  found  the  anatomical 
changes  produced  by  the  disease  to  which  the  endocarditis  is  sec- 
ondary, since  it  is  extremely  rare  to  find  it  as  an  independent  dis- 


150  DISEASES  OF  THE   HEART 

ease.  It  is  very  often  associated  with  the  chronic  form  of  endo- 
carditis. 

The  secondary  changes  in  the  simple  form  are  trifling,  and  as 
a  rnle  produce  no  symptoms.  It  is  only  in  the  conrse  of  time, 
when  the  disease  passes  into  the  chronic  form,  that  serious  damage 
is  done.  Secondary  to  the  malignant  form,  on  the  contrary,  are 
circulatory  disturbances  consequent  on  the  ulceration  or  perfora- 
tion of  the  valves,  and  more  important  still,  the  metastatic  foci  of 
disease  set  up  all  over  the  body  by  means  of  septic  emboli.  The 
spleen  and  kidney  are  especially  apt  to  suffer  in  this  way.  The 
infarcts  so  produced  may  be  few,  or  innumerable  muiide  foci  of 
suppuration  may  be  scattered  over  the  whole  body.  It  is  to  these 
septic  emboli  that  this  form  of  the  disease  owes  its  malignant 
character. 

Etiology. — It  may  be  stated  as  a  general  proposition,  that  the 
bacterial  origin  of  acute  endocarditis,  both  simple  and  ulcerative, 
has  been  established.  Heiberg's  discovery  in  1872  of  micrococci 
in  the  thrombotic  masses  of  the  malignant  form  has  led  to  an 
unbroken  series  of  researches  and  experiments  by  the  most  bril- 
liant pathologists  in  Europe  and  this  country,  with  the  result 
that  the  cloud  of  doubt  and  speculation  once  enveloping  this  sub- 
ject has  at  length  been  cleared  away.  Special  activity  in  this 
work  was  displayed  during  the  years  immediately  following  1885, 
and  prominently  figuring  in  this  line  of  investigation  are  the 
names  of  Virchow,  Klebs,  Birch-Hirschfeld,  Koester,  Weichsel- 
baum,  Fraenkel  and  Saenger,  Ilosenbach  and  T^etter  in  Germany; 
Gilbert  and  Lion,  Cornil  and  Babes,  Ivoux,  Josseraut,  ^nd  Dessy, 
in  France;  Dreschfeld,  Cayley,  Purser,  in  England;  Osier,  Flex- 
ner,  and  Prudden  in  this  country.  It  is  manifestly  .impossible 
within  the  limits  of  this  work  to  give  a  detailed  account  of  the 
nature  of  the  researches  made  by  these  eminent  workers,  and  it 
must  suffice  to  state  the  facts  that  have  been  established. 

Micro-organisms  have  been  quite  generally  found  in  cases  of 
malignant  endocai^ditis,  some  of  them  being  the  same  as  those 
found  in  other  infectious  diseases,  a  few  being  specific  to  endo- 
carditis. Occasionally  two  or  more  varieties  have  existed  in  the 
same  case.  The  bacteria  most  usually  discovered  have  been  strep- 
tococcus pyogenes,  ])articularly  of  erysipelas;  staphylococcus 
pyogenes,   aureus,    and   albus,   and   the  micrococcus   lanceolatus. 


ACUTE  ENDOCARDITIS  151 

The  gonococcus,  the  bacilhis  of  typhoid  fever,  of  diphtheria,  of  in- 
fluenza, and  of  tuberculosis  have  also  been  found,  although  much 
less  frequently. 

Weichselbaum  identified  certain  bacteria,  which,  because  they 
appear  to  occur  only  in  endocarditis,  he  named  bacillus  endocar- 
ditidis  griseus  and  capsulatus  and  micrococcus  endocarditidis 
rugatus.  The  bacillus  immobilis  et  fostidus  was  also  found  by 
Fraenkel  and  Saenger.  That  these  various  bacteria  are  capable  of 
inducing  endocarditis  has  been  shown  by  experimentation  on  ani- 
mals. A  number  of  investigators  injected  pure  cultures  of  micro- 
organisms obtained  from  infected  valves  into  the  jugular  veins  of 
dogs  and  rabbits,  and  afterward  found  these  cocci,  often  in  masses, 
both  on  the  surface  and  in  the  deeper  layers  of  both  aortic  and 
mitral  valves,  the  valves  themselves  showing  characteristic  inflam- 
matory changes.  By  some  experimenters  it  was  asserted  that 
endocarditis  could  be  only  thus  produced  after  the  valves  had  suf- 
fered trauma  by  chemical  or  mechanical  irritation.  Others,  on 
the  contrary,  claimed  to  have  produced  endocarditis  by  injection 
of  microbes  into  animals  without  previous  injury  of  the  endo- 
cardium. 

In  numerous  instances  the  bacteria  found  on  the  affected 
valves  have  also  been  identified  in  the  septic  emboli  thro^vn  off 
during  the  course  of  the  disease,  while  in  a  few  instances  the 
blood  of  patients  suffering  from  infective  endocarditis  has  been 
found  to  contain  septic  organisms. 

The  bacteria  found  in  the  lesions  of  ulcerative  endocarditis 
occurring  as  a  complication  of  typhoid  fever  and  diphtheria  are 
usually  pyogenic.  This  is  also  true  of  most  cases  of  gonorrhoeal 
endocarditis,  although  the  gonococcus  has  been  definitely  identi- 
fied in  the  endocarditic  lesions.  .  The  pneumococcus  of  Fraenkel 
has  been  frequently  found  in  endocarditis,  both  simple  and  ulcera- 
tive, but,  according  to  Osier,  more  frequently  in  the  latter  variety. 

It  appears  well  established  that  a  primary  endocarditis  of  bac- 
terial origin  is  occasionally,  although  rarely,  met  with.  Most  in- 
stances of  endocarditis  are  secondary  to  some  general  or  local  in- 
fection. 

There  has  been  considerable  speculation,  and  for  a  time  there 
was  a  heated  discussion,  particularly  between  Klebs  and  Koester, 
over  the  route  by  which  microbes  are  carried  to  the  infected  valves. 


152  DISEASES  OP  THE  HEART 

Klebs  and  \'ircliow  inaiiitaiiied  they  were  (l('])ositod  on  the  surface 
of  the  cvisps  ont  of  the  blood,  while  Koester  declared  they  were 
carried  thither  in  the  niinnte  capillaries  situated  in  the  deeper 
layers  of  the  valves.  He  maintained  that  the  masses  of  cocci 
caused  embolic  plugging  of  the  vessels,  which  was  followed  by  rup- 
ture, thus  setting  free  the  bacteria  and  allowing  them  to  reach  the 
surface.  x\gainst  this  explanation  was  urged  the  scarcity  of  blood- 
vessels in  the  valves,  as  well  as  the  fact  that  the  earliest  evidence 
of  inflammatory  change  is  along  the  line  of  contact  of  the  cusps. 
It  is  now  held  that  both  contentions  are  correct,  but  Virchow's 
view  is  accepted  by  the  majority  of  observers.  The  adherents  of 
Virchow's  opinion  believe  that  the  pressure  of  the  blood  forces  the 
micro-organisms  between  the  endothelial  cells  of  the  endocardium 
— a  theory  that  probably  accounts  for  the  develoi)ment  of  endocar- 
ditis in  the  left  heart  after  birth  and  in  the  right  side  during 
fa3tal  existence.  As  is  well  known,  blood-pressure  is  greater  in  the 
right  ventricle  before  and  in  the  left  ventricle  after  birth. 

Another  explanation  for  the  localization  of  endocarditis  is  that 
inasmuch  as  oxygen  is  necessary  to  the  growth  and  activity  of  most 
bacteria,  these  organisms  are  most  active  in  blood  relatively  rich  in 
oxygen,  a  condition  obtaining  in  the  right  cardiac  chambers  in  the 
foetus  and  in  the  left  during  extra-uterine  existence, 

A  most  interesting  question  relates  to  those  conditions  that  de- 
termine whether  the  endocarditis  is  to  be  simple  or  ulcerative, 
since  both  forms  are  of  microbic  origin,  and .  some  of  the  same 
organisms  have  been  found  in  the  endocarditic  vegetations  of  both 
varieties,  What  are  the  factors  that  determine  the  malignancy  or 
benignity  of  the  affection  ?  It  has  been  suggested  that  this  de- 
pends upon  the  number  of  bacteria  present.  It  is  more  probable, 
however,  that  when  healthy  valves  are  attacked  the  nature  of  the 
endocarditis  depends  upon  th(;  virulence  of  ihv  infecting  organ- 
isms. Other  factors  are  of  influence,  however,  aside  from  the 
nature  or  virulence  of  the  bacteria,  and  these  will  now  be  con- 
sidered. 

Simple  Endocarditis. — Articular  rheumatism  is  the  disease  par 
excellence  in  which  acute;  sim])l(!  endocarditis  is  most  frequently 
observed. 

Why  this  is,  is  not  as  yet  satisfactorily  established,  but  there 
appears  to  be  a  growing  belief  among  pathologists  in  the  bacterial 


ACUTE   ENDOCARDITIS  153 

origin  of  rheumatism,  as  opposed  to  the  once  prevalent  notion  of 
its  dependence  upon  lactic  acid  in  the  blood.  The  relative  fre- 
quency with  which  these  two  affections  are  associated  is  variously 
estimated.  Of  32  cases  of  inflammatory  rheumatism  that  termi- 
nated fatally,  Fagg  found  the  valves  affected  in  all  but  12.  Ac- 
cording to  Hayden,  Peacock  found  endocarditis  in  16  per  cent  of 
his  cases  of  rheumatism,  while  Fagg  puts  the  ratio  as  high  as  40  or 
50  per  cent.  French  as  well  as  English  observers  put  the  propor- 
tion much  higher  than  do  the  Germans;  thus  Bouillaud,  55  per 
cent ;  Budd,  48  per  cent ;  Fuller,  23  per  cent ;  while  Wunder- 
lich  and  Lebert  give  it  as  23  per  cent,  and  Bamberger  20  per  cent. 
These  differences  probably  depend  upon  the  severity  of  the  rheu- 
matic attack,  since  all  observers  agree  in  the  statement  that  the 
valves  are  far  more  likely  to  become  inflamed  in  acute  than  in  sub- 
acute or  chronic  forms  of  articular  rheumatism.  Endocarditis  is 
especially  liable  to  occur  in  a  first  attack  of  arthritis,  particularly 
when  this  is  severe  and  several  joints  are  involved.  There  is  no 
doubt,  however,  of  its  development  as  a  result  of  subacute  or 
chronic  rheumatic  manifestations.  Hayden  is  of  the  opinion  that 
in  rare  instances  endocarditis  may  be  the  only  manifestation  of  the 
rheumatic  poison.  The  period  in  the  course  of  acute  rheumatism 
at  which  endocarditis  may  occur  is  given  by  Hayden  from  the 
sixth  to  the  ninth  day,  and  by  Fuller  as  from  the  sixth  to  the 
twentieth  day.  The  earlier  the  time  of  life  at  which  acute  rheu- 
matism develops,  the  greater  is  its  liability  to  set  up  acute  endo- 
carditis. 

The  next  most  frequent  predisposing  cause  of  this  form  of  en- 
docardial inflammation  is  generally  stated  to  be  chorea.  Endo- 
carditis of  this  origin  is  numerically  less  frequent  than  the  rheu- 
matic, whereas  the  relative  frequency  of  chorea  and  endocarditis 
is  thought  by  some  observers  to  be  greater ;  thus,  of  16  cases  of  fatal 
chorea  occurring  at  Guy's  Hospital  during  twenty  years,  Fagg 
found  post-mortem  evidence  of  endocarditis  in  14.  Here,  again, 
there  has  been  much  speculation  concerning  the  reason  of  the  asso- 
ciation between  chorea  and  endocarditis.  By  some  the  latter  is 
attributed  to  acute  articular  rheumatism,  which  is  now  recognised 
to  be  frequently  associated  with  chcrea.  Thus  in  40  cases  of  the 
latter  affection  manifesting  organic  heart-disease,  Gowers  found  in 

all  a  trustworthy  history  of  associated  rheumatism.     There  are 

12 


154  DISEASES  OF  THE  HEART 

some  observers,  on  the  other  liand,  who  hold  that  chorea  is  capable 
of  causing  endocarditis  independently  of  associated  or  antecedent 
arthritis.  Since  girls  are  undeniably  more  subject  to  chorea  than 
are  boys,  endocarditis  of  this  origin  is  observed  more  frequently  in 
the  former  sex. 

Scarlatina  and  measles  are  also  accredited  with  the  causation 
of  endocardial  inflammation.  This  may  be  either  a  secondary  re- 
sult, or  the  endocarditis  may  be  due  to  a  mixed  infection.  Inas- 
much, however,  as  scarlet  fever  is  not  infrequently  followed  by 
rheumatic  manifestations,  the  endocarditis  is  held  by  some  to  be 
referable  to  the  latter  and  not  to  the  former  affection. 

Other  irruptive  diseases,  particularly  enteric  fever  and  small- 
pox, are  also  capable  of  setting  up  endocarditis,  but  as  subse- 
quently stated,  this  is  more  likely  to  be  malignant  than  merely 
simple. 

Although  gonorrha^a  is  more  likely  to  cause  the  ulcerative 
form,  vegetative  endocarditis  undoubtedly  occurs  as  a  result  of 
gonococcus  or  perhaps  a  mixed  infection,  a  conclusion  that  would 
seem  justified  by  the  entire  absence  of  any  other  etiological  factor 
in  certain  cases  of  valvular  disease. 

As  previously  stated,  there  is  both  clinical  and  pathological 
evidence  of  the  occurrence  of  acute  endocarditis  in  the  course  of 
croupous  pneumonia  or  in  consequence  of  pneumoeoecus  infection. 
Although  such  an  endocarditis  is  more  likely  to  be  ulcerative,  it 
may  nevertheless  be  benign.  In  a  fatal  case  of  pneumonia,  which 
had  exhibited  no  evidences  of  endocarditis  during  life,  Haushalter 
found  a  colony  of  pneumococci  in  the  interior  of  one  of  the  mitral 
cusps,  while  the  otlior  showed  an  almost  invisible  swelling  of  the 
endothelium  near  the  point  of  insertion  of  the  valve.  From  this 
he  concluded  that  not  only  is  acute  endocarditis  a  probable  se- 
quence of  pneumonia,  but  also  endocarditic  changes  of  a  slow 
sclerotic  type  may  be  ultimately  set  up.  His  conclusions  were  as 
follows:  (1)  The  absence  of  murmurs  during  life  or  of  naked  eye 
changes  post  mortem  does  not  j)rove  the  integrity  of  the  valve, 
since  during  the  course  of  the  pneumonia  the  pathogenic  organ- 
isms may  be  carried  into  the  interior  of  the  valve,  and  thus  prove 
the  starting-point  of  future  valvular  mischief.  (2)  The  possi- 
bility of  such  an  endocarditis  should  be  remembered,  since  a  latent 
period  may  exist  between  the  primary  disease  and  the  develop- 


ACUTE  ENDOCARDITIS  155 

ment  of  the  endocarditis.  (3)  The  possibility  of  such  an  occur- 
rence renders  it  advisable  for  the  physician  to  keep  a  patient  under 
prolonged  observation  after  recovery  from  pneumonia,  and  to 
make  repeated  examinations  of  the  heart,  that  he  may  thereby 
detect  the  earliest  manifestations  of  a  valvular  lesion. 

Injury  of  the  valves  through  strain  is  generally  recognised  as 
one  of  the  conditions  predisposing  to  the  occurrence  of  acute  endo- 
carditis. By  some  it  is  contended,  however,  that  strain  alone  is 
not  sufficient,  but  must  be  united  with  some  previously  existing 
defect.  Strain  is  probably  capable  of  setting  up  fresh  inflamma- 
tion of  a  valve,  already  the  subject  of  a  former  though  slight  endo- 
carditis. Rupture  of  a  cusp  may  undoubtedly  prove  a  starting- 
point  of  acute  inflammatory  change. 

Age  is  an  undoubted  predisposing  factor,  acting  in  most  cases, 
however,  in  the  way  of  rendering  individuals  susceptible  to  articu- 
lar rheumatism,  the  exanthemata  or  other  diseases,  themselves 
capable  of  bringing  about  endocarditis.  Supporting  this  view  or 
interpretation  of  the  influence  of  age  is  the  statement  that  rheu- 
matism is  more  likely  to  occasion  endocarditis  in  childhood  than 
in  the  later  periods  of  life.  Both  sexes  are  liable  to  endocarditis, 
yet  according  to  some  this  affection  is  more  frequent  among  fe- 
males, although  males  are  said  to  be  more  subject  to  articular 
rheumatism.  To  my  mind  there  is  nothing  in  sex,  per  se,  render- 
ing the  endocardium  more  vulnerable  in  females  than  it  is  in 
males. 

Females  are  more  subject  to  chorea  and,  by  reason  of  their 
sex,  to  puerperal  septicaemia  and  infections  from  pelvic  disease, 
and  hence  it  may  well  be  that  they  furnish  a  greater  numerical 
proportion  of  cases  of  acute  endocarditis,  benign  as  well  as  ulcera- 
tive. With  increasing  experience,  I  find  myself  growing  in  the 
conviction  that  hereditary  influence  plays  a  not  unimportant  role 
in  the  development  of  endocardial  disease.  Cardiac,  and  particu- 
larly valvular  lesions,  as  such,  cannot  be  inherited,  but  it  seems  to 
me  that  in  some  families  whose  members  evince  pronounced  rheu- 
matic diathesis,  there  is  an  inherent  vulnerability,  possibly  heredi- 
tary, of  the  endocardium  in  the  presence  of  rheumatism. 

Ulcerative  Endocarditis. — It  is  a  well-known  fact,  established 
both  by  clinical  and  post-mortem  observation,  that  the  malignant 
form  is  particularly  prone  to  .develop  as  the  result  of  fresh  bacte- 


156  DISEASES  OF   THE   HEART 

rial  invasion  in  valves  already  the  seat  of  chronic  endocarditis  or 
sclerotic  change.  This  is  particidarly  trne  of  the  aortic-valve 
apparatus. 

Infections  endocarditis  is  also  specially  liable  to  attack  indi- 
viduals suffering  from  exhausting  diseases  or  cachexiie,  chronic 
alcoholism,  cirrhosis  of  the  liver,  hepatic  abscess,  cancer,  etc. 

General  infection,  as  pyannia,  puerperal  septicaemia,  influenza, 
diphtheria,  variola,  and  localized  septic  processes  or  abscesses, 
predispose  to  malignant  rather  than  to  simple  endocarditis.  Flex- 
ner  found  stai)hylococcus  aureus  in  a  case  of  endocarditis  in  which 
the  atrium  of  infection  was  leg  ulcer;  in  another,  staphylococcus, 
the  point  of  entrance  being  the  intestine ;  in  still  another,  strepto- 
coccus and  staphylococcus,  the  atrium  being  hepatic  abscess.  This 
form  of  acute  endocarditis  has  been  particularly  frequent  in  asso- 
ciation with  puerperal  septictemia  due  to  infection  either  of  the 
uterus  or  its  adnexa.  It  has  been  known  to  follow  tonsillitis,  and 
even  so  apparently  trivial  a  local  process  as  a  furuncle. 

Croupous  pneumonia  or  a  pneumococcus  meningitis  has  not 
infrequently  been  found  as  the  prinuiry  infection  in  cases  of  ulcer- 
ative endocarditis.  Although  the  pneumococcus  may  occasionally 
give  rise  to  the  simple  form,  it  is  much  more  frequently  respon- 
sible for  ulcerative  inflammation  of  the  valves.  This  malignant 
form  is  also  stated  by  Dreschfeld  to  have  been  associated  with  7 
cases  of  gall-stones  "  with  or  without  suppuration  of  the  biliary 
passages."  Dreschfeld  thinks  that  the  discovery  of  the  bacterium 
coli  commune  in  diseases  of  the  biliary  passages  may  explain  their 
connection  with  acute  endocarditis.  In  this  connection  it  is  inter- 
esting to  note  that  Flexner,  in  one  case  of  endocarditis  associated 
with  carcinoma  of  the  pylorus,  identified  the  bacillus  coli,  together 
with  the  bacillus  pyocyaueus ;  and  Ilasenfeld  has  reported  arti- 
ficially produced  endocarditis  in  animals  infected  with  the  bacillus 
pyocyaneus.  Of  further  interest  is  the  fact  that,  despite  the  severe 
infectious  process,  distinct  hy])ertro])hy  of  the  heart  was  observed 
to  develop  in  so  sliort  a  time  as  a  week. 

Finally,  this  form  of  endocarditis,  although  much  less  fre- 
quently than  the  siiiii)l(',  nuiy  exist  in  connection  with  articular 
rheumatism,  as  mentioned  by  Osier  and  others. 

Its  dependence  upon  the  di])htheria  bacillus,  though  rare,  is 
undoubted.     Howard  has  rej)orted  a  case  in  which  a  bacillus  was 


ACUTE  ENDOCARDITIS  157 

discovered  identical  in  all  respects  with  tlie  Klebs-Loeffler  bacillus. 
It  is  now  generaly  recognised  that  septic  endocarditis,  although 
capable  of  being  set  up  by  pathogenic  organisms,  is  most  fre- 
quently caused  by  streptococci  and  staphylococci. 

Symptoms. — Just  as  it  is  sometimes  difficult  from  a  patho- 
logical standpoint  to  say  whether  the  soft,  easily  detached  thrombi 
belong  to  the  vegetative  or  infective  variety,  so  a  sharp  dividing 
line  cannot  always  be  drawn  clinically  between  the  two  forms  of 
endocarditis.  Nevertheless,  I  think  it  will  conduce  to  clearness 
if,  as  is  usually  done,  they  are  described  separately. 

Acute  Simple  Endocarditis. — As  this  process  frequently  occurs 
in  the  course  of  articular  rheumatism,  of  which  it  may  be  regarded 
as  a  manifestation,  and  not  a  convplication,  its  symptoms  are  often 
masked  by  those  of  the  arthritis.  If  the  endocarditis  be  of  a  mild 
type,  it  may  pursue  a  latent  course,  and  only  be  detected  by  its 
results  when  years  subsequently  the  individual  is  found  to  have  a 
valvular  lesion,  probably  dating  back  to  some  almost  forgotten 
rheumatic  attack.  Such  a  possibility  should  always  be  borne  in 
mind  by  any  physician  attending  a  case  of  articular  rheumatism, 
however  mild,  and  should  incite  him  to  a  daily  examination  of 
the  heart,  since  many  times  acute  endocarditis  is  only  recognisable 
by  such  means. 

If  in  the  course  of  rheumatic  fever,  especially  towards  the 
end  of  the  first  week,  the  temperature  unexpectedly  rises,  and  can- 
not be  accounted  for,  by  involvement  of  a  fresh  joint  or  some  com- 
plication, attention  should  be  at  once  fastened  upon  the  heart.  If 
the  endocardium  has  become  inflamed,  with  or  without  implica- 
tion of  the  pericardium,  the  fact  will  eventually  declare  itself  by 
the  physical  signs  subsequently  to  be  described,  even  though  sub- 
jective symptoms  are  wanting. 

In  some  cases  subjective  symptoms  become  manifest  from  the 
start,  and  are  then  due  probably  either  to  the  severity  of  the  endo- 
carditis or  to  associated  myocarditis  or  pericarditis.  These  symp- 
toms are  pr^ecordial  pain  more  or  less  pronounced,  or  an  ill-de- 
fined sense  of  oppression  and  discomfort  in  the  cardiac  region,  pal- 
pitation, the  heart-action  in  some  cases  being  quite  tumultuous, 
and  particularly  a  subjective  sense  of  dyspnoea.  By  this  term  is 
meant  a  sensation  on  the  part  of  the  patient  of  air-hunger,  which 
may  not  be  evinced  by  laboured  or  hurried  respiration,  but  which 


158  DISEASES  OF  THE   HEART 

is  usually  greater  than  can  be  accounted  for  upon  examination  of 
the  chest.  I  cannot  now  recall  a  single  case  of  acute  endocarditis, 
recognised  as  such,  in  which  this  symptom  was  not  present.  In 
some  instances  this  feeling  of  breathlessness  actually  amounts  to 
orthopna-a ;  in  others  dyspnoea  is  paroxysmal,  compelling  the  pa- 
tient to  sit  up  in  bed  during  the  continuance  of  the  paroxysm.  In 
mild  cases  the  pyrexia  is  likely  to  be  mild,  and  possesses  no  pecu- 
liar character. 

In  other  instances  the  disease  produces  profound  constitutional 
disturbances,  with  fluctuating  fever  and  profuse  perspiration, 
plainly  suggesting  infection,  and  with  a  pulse  so  empty,  irregular, 
and  perhaps  accelerated,  as  to  at  once  direct  the  physician's  atten- 
tion to  the  heart.  These  are  the  eases  difficult,  if  not  impossible, 
of  differentiation  from  the  malignant  form. 

Embolic  phenomena  are  less  frequent  in  the  benign  than  in 
the  malignant  form,  yet  when  embolisms  occur  the  symptoms  they 
induce  are  referable  to  mechanical  interference  with  the  circula- 
tion, rather  than  to  a  local  or  general  septic  process.  The  most 
usual  seat  of  infarcts  is  in  the  kidney,  intestines,  and  brain.  They 
undoubtedly  occur  many  times  without  giving  rise  to  recognisable 
symptoms ;  yet  when  such  are  produced,  they  are  a  sudden,  sharp 
pain  in  the  affected  part  or  organ,  chill  more  or  less  pronounced, 
and  pyrexia.  If  the  embolus  lodge  in  a  kidney  the  urine  is  likely 
to  contain  blood,  albumin,  and  even  i)us.  Hemiplegia  and  aphasia, 
the  result  of  cerebral  embolism,  may  in  rare  instances  furnish  the 
first,  or  perhaps  the  conclusive,  evidence  of  the  existence  of  acute 
endocarditis.  The  following  case  is  instructive:  W.  J.  M.,  male, 
aged  forty-eight  years,  height  six  feet,  weight  176  pounds,  first 
consulted  me  November  9,  1896,  not,  he  said,  because  he  thought 
himself  in  poor  health,  but  because,  having  some  heart-trouble, 
a  friend  advised  him  to  get  my  opinion.  Family  history  was  un- 
important in  its  bearings  upon  the  patient's  condition,  but  it  was 
stated  that  one  sister  had  died  of  consumption,  another  of  insanity, 
and  a  third,  then  living,  had  heart-disease.  Patient  declared  that 
he  had  not  been  ill  since  his  twelfth  year,  but  had  had  syphilis 
at  the  age  of  twenty.  After  his  death,  it  was  stated  by  his  wife 
that  the  patient  had  known  for  seven  years  of  the  existence  of 
some  sort  of  heart-disease.  Symptoms  such  as  dyspnoea  and 
palpitations    were    denied,    but    the    patient,    when    questioned 


ACUTE  ENDOCARDITIS 


159 


regarding  pain,  said,  "  Once  in  a  while  a  little,  down  near  the 
heart." 

The  pnlse  was  noted  as  89,  not  distinctly  collapsing,  the  left 
seeming  slightly  smaller.  Carotids  and  subclavians  throbbed 
stronglj^  Apex-beat  in  sixth  left  intercostal  space,  3f  inches  from 
the  sternum,  and  the  cardiac  impulse  was  heaving ;  diffused  from 
the  fifth  to  the  seventh,  but  maximum  in  the  sixth  interspace. 
Absolute  cardiac  dulness  was 
practically  normal,  but  the 
relative  was  increased  to  the 
left,  extending  5|  inches  to 
the  left  of  the  breastbone, 
downward  to  the  seventh  rib, 
•and  but  1  inch  to  the  right  of 
the  sternum  (Fig.  28).  The 
first  sound  at  apex  was  muiSed 
and  the  second  was  wanting; 
throughout  the  pr?ecordium 
the  sounds  were  obscured  by 
murmurs,  both  systolic  and 
diastolic,  which  were  audible 
over  the  entire  cardiac  area, 
but  were  of  maximum  inten- 
sity in  the  aortic  area  and  on 
the  body  of  the  sternum.  A 
snapping  systolic  tone  was  audible  in  the  femoral  artery.  In  the 
aortic  area  bimanual  palpation  with  slight  pressure  brought  out 
a,  systolic  shock  and  thrill.  Examination  of  abdomen  and  urine 
was  negative. 

The  diagnosis  lay  between  aneurysm  of  the  ascending  aorta 
and  insufficiency  of  the  aortic  valves,  but  the  lesion  was  subse- 
quently decided  to  be  a  valvular  one  of  sclerotic,  possibly  syphilitic 
origin. 

For  the  next  few  months  the  patient  was  seen  at  rather  iiifre- 
quent  intervals  until  the  last  of  March,  1897.  In  February  of 
that  same  year  patient  was  knocked  down  by  a  runaway  horse, 
but  did  not  think  he  sustained  special  injury.  Towards  end  of 
March  he  began  to  complain  of  insomnia,  great  nervousness,  and 
restlessness.     The  heart  was  rapid  and  pounding,  and  there  was 


Fig.    28. — Apex-beat    and    Relative    Dul- 
ness, Case  of  Acute  Endocarditis  (p. 

158). 


160  DISEASES  OF  THE  HEART 

dyspnoea,  even  in  repose,  which  increased  paroxysmallv  without 
cause.    Urine  analysis  showed  pus,  blood,  and  albumin. 

Patient  was  ordered  to  keep  to  the  house  and  confine  himself 
to  milk  diet,  with  potassium  citrate  and  tincture  of  digitalis  in 
small  doses,  with  saline  cathartics  daily.  After  about  two  months 
the  urine  lost  all  traces  of  blood  and  albumin,  but  patient's  gen- 
eral condition  grew  worse,  and  he  was  ordered  to  keep  his  bed. 
Heart's  action  was  still  rapid  and  pounding,  but  regidar,  and  dysp- 
noea with  paroxysmal  exacerbations  very  marked.  Patient  sweated 
profusely,  but  the  thermometer  never  showed  fever. 

One  night  complained  of  pain  in  right  hypochondrium  below 
ribs,  embolism  was  suspected,  but  subsequently  doubted.  Liver 
reached  3  fingers  below  costal  arch,  was  moderately  tender,  firm, 
and  with  rounded  border.  The  condition  was  thought  to  be  pass- 
ive congestion  without  infarction.  About  the  last  of  May  patient 
developed  mental  symptoms,  as  shown  by  ugliness  of  temper,  espe- 
cially towards  wife;  it  appeared  to  be  a  mild  acute  mania,  and 
the  wife  stated  that  the  mother  as  well  as  a  sister  had  died  insane. 
Hyoscine  hydrobromate  w^as  ordered,  supplemented  subsequently 
by  valerianate  of  ammonia,  with  improvement,  the  delirium  being- 
only  occasional  and  ugliness  less. 

June  2,  1897,  examination  showed  the  following:  Radial  pulse 
distinctly  collapsing,  venous  pulsation  in  forearm,  but  external 
jugulars  not  turgid  and  without  pulsation.  Apex-beat  in  sixth 
left  interspace,  anterior  axillary  line,  systolic  impulse  in  second 
and  third  right  interspaces  near  sternum,  followed  by  diastolic 
thrill,  also  a  more  feeble  pulsation  in  fourth,  fifth,  and  sixth  right 
interspaces,  slight  systolic  shock  in  second  left  interspace  near 
sternum.  Absolute  dulness,  patient  in  dorsal  decubitus,  reached 
6  centimetres  to  right  of  median  line,  and  from  second  to  sixth 
costal  cartilage,  the  note  being  flat,  with  marked  resistance  from 
second  rib  to  fourth  interspace,  and  slightly  less  dull  below  this 
point.  Dulness  also  reached  10.5  centimetres  to  left  of  median 
line  (Fig.  29). 

Auscultation  showed  first  sound  at  apex,  dull  and  muffled,  but 
no  distinct  murmur,  a  double  tone  audible  below  left  clavicle  and 
down  along  left  axillary  line;  a  systolic  tone  and  soft  diastolic 
murmur  in  second  left  interspace  and  outward  li  inch  from  ster- 
num.    Tlicrc  wiis  also  a  faint  second  sound  in  the  ])nlmonary  area^ 


ACUTE   ENDOCARDITIS 


161 


and  when  the  patient  took  a  Jeep  inspiration  and  held  his  breath 
the  second  sound  seemed  to  be  changed  into  a  soft  murmur. 

The  soft  diastolic  murmur  at  left  of  sternum  was  transmitted 
faintly  downward.  A  painfully  loud  and  harsh  diastolic  and 
systolic  murmur  was  heard  in  second  and  third  right  interspaces, 
and  transmitted  more  feebly  into  fifth,  out  to  nipple  and  up  to 
neck. 

The  condition  was  interpreted  as  follows :  Acute  endocarditis 
ingrafted  on  a  chronic  endocarditis,  affecting  aortic  valves  and 
aorta,  and  producing  dilatation  of  this  vessel.  jSTo  evidence  could 
be  found  of  inflammation  of  other  valves,  and  yet  the  great  extent 
of  dulness  to  right  of  sternum  was  thought  due,  in  addition  to 
aortic  dilatation,  to  dilata- 
tion of  the  right  auricle,  sec- 
ondary ito  mitral  insufiiciency. 
Cough  was  at  no  time  a 
marked  symptom,  except  two 
or  three  paroxysms  a  few 
hours  before  death,  when 
patient  seemed  to  have  pain  in 
left  lung.  During  the  last 
few  weeks  of  life  there  was 
moderate  cedema  of  ankles  and 
shins,  also  puffiness,  but  no 
pain,  in  left  wrist  and  hand. 
Forty-eight  to  sixty  hours  be- 
fore death  patient  became 
comatose,  with  cold  extremi- 
ties, very  rapid,  feeble,  and 
irregular  pulse,  and.  the  trunk  and  lower  extremities  became 
studded  with  small  brownish-red  spots,  that  had  all  the  characters 
of  cutaneous  embolisms.  Death,  which  took  place  June  24th, 
seemed  to  be  the  result  of  gradual  cardiac  asthenia. 

The  autopsy,  made  by  Dr.  W.  A.  Evans  thirteen  hours  after 
death,  was  briefly  as  follows:  Very  large  numbers  of  petechia? 
over  abdomen,  chest,  and  legs,  about  the  size  of  a  pea.  Some  inter- 
stitial splenitis  and  perisplenitis  and  zones  of  connective-tissue 
growths  representing  old  infarcts.  These  were  generally  subcap- 
sular. 


Fig.    29. — Apex-beat   and    Absolute    Dul- 
ness Later  in  Same  Case  as  Fig.  28. 


162  DISEASES  OP  THE  HEART 

Liver. — Fatty  infiltration — nutmeg.  Large  numbers  of  small 
islands  of  connective-tissue  increase,  quite  generally  distributed 
in  subcapsular  zone.  A  small  mass  of  calcareous  material  in  lower 
portion  of  right  lobe,  superficial.  In  left  lobe  a  small  fresh  in- 
farct about  6  millimetres  in  diameter. 

Left  Kidney. — Slight  parenchymatous  nephritis. 

Right  Kidney. — In  the  cortex  an  old  infarct  1  centimetre  in 
diameter,  over  this  the  surface  of  the  kidney  depressed.  This  in- 
farct, fatty  in  appearance,  reddish,  surrounded  by  a  reddish  zone. 
It  was  this  infarct  which  in  March  had  occasioned  the  bloody  and 
albuminous  urine. 

Left  Pleural  Cavity. — ^o  fluid,  no  adhesions  except  to  dia- 
phragm. 

Left  Lung. — Congested  and  oedematous.  In  anterior  edge  of 
inferior  lobe  an  apoplectic  focus  about  1  centimetre  in  diameter, 
quite  recent. 

Right  Pleural  Cavity. — Extensive  old,  firm,  fibrous  adhesions 
quite  general. 

Right  Lung. — Congested  and  (edematous,  single  ha?morrhagic 
infarct  2  centimetres  in  diameter. 

Pericardium. — I^o  effusion,  uniform  adhesions  between  peri- 
cardial layers.     They  strip  easily,  appear  gelatinous  or  mucoid. 

Aorta. — Tubular  dilatation  of  aorta  in  its  first  portion.  The 
lumen  is  somewhat  ovoid,  measuring  9  by  8  centimetres.  The 
aortic  ostium  dilated  with  compensatory  stretching  of  the  aortic 
cusps.  The  aortic  cusps,  measured  along  their  free  edge,  show  a 
length  of  5  centimetres,  4^  centimetres,  and  3^  centimetres  re- 
spectively. All  of  the  cusps  show  ridges  of  atheroma,  with  con- 
siderable thickening  and  stiffening.  At  the  base  of  the  largest 
cusp,  a  calcareous  plate.  Thickening,  redness,  and  some  deposit 
of  fibrin  on  each  of  the  cusps,  especially  towards  the  free  edge. 

The  valves  not  competent.  Aorta  atheromatous.  Areas  of 
calcification,  atheromatous  ulcers,  and  some  vegetations  around 
these  losses  of  substance.  The  left  ventricle  enormously  dilated, 
its  wall  .J  centimetres  in  thickness  at  its  thickest  portion.  Myo- 
cardium is  not  especially  fatty.  Mitral  valves  show  multiple 
foci  of  acute  endocarditis,  consisting  of  small,  round  red  masses, 
the  size  of  a  pin-head. 

Left  auricle  very  much  dilated,  right  heart  otherwise  normal. 


ACUTE   ENDOCARDITIS  163 

Oultiires  made  from  the  vegetations  give  no  growth  of  micro- 
-organisms. 

Diagnosis. — Tubular  aneurysm  first  portion  of  aorta ;  ather- 
oma of  aorta  and  aortic  cusps ;  hypertrophy  and  dilatation  of  the 
left  heart ;  acute  endocarditis  and  endaortitis,  vegetative  in  char- 
acter.    Recent  infarcts  in  liver  and  lungs. 

This  case  illustrates  the  proneness  of  acute  inflammation  to 
attack  valves  that  have  undergone  sclerotic  changes.  It  is  prob- 
able that  the  aortic  regurgitation  diagnosed  in  the  fall  of  1896 
was  due  partly  to  incompetence  of  the  cusps  from  stiffening  and 
rigidity  and  partly  to  stretching  of  the  ring  consecutive  to  the  dila- 
tation of  the  ascending  aorta,  the  valves  not  being  able  to  ade- 
quately close  the  ostium  in  spite  of  their  compensatory  stretching. 
With  the  exception  of  the  lack  of  febrile  temperature  the  symp- 
toms strongly  suggested  ulcerative  endocarditis,  and  show  how 
difficult  and  unwise  it  is  to  attempt  a  sharp  clinical  distinction 
between  the  two  forms  of  endocarditis.  The  anatomical  changes 
were  those  of  the  vegetative  variety,  and  yet  in  its  rapid  course 
and  fatal  termination  the  process  may  be  said  to  have  been  ma- 
lignant. 

Course  and  Termination. — As  already  stated,  in  some 
■cases  rheumatic  endocarditis  of  a  mild  type  may  be  easily  distin- 
guished from  infective  endocarditis,  while  other  cases  seem  to 
■occupy  intermediate  ground,  and  clinically,  at  least,  cannot  be 
classed  with  either  one  or  the  other  type.  It  is  plain,  therefore, 
that  the  course  and  termination  are  equally  variable. 

Simple  rheumatic  endocarditis  may  pursue  a  favourable 
'Course,  and  terminate  in  the  recovery  of  the  patient,  nay,  may  even 
subside  without  serious  impairment  of  the  affected  valve.  In  the 
majority  of  cases,  however,  the  patient  is  usually  left  with  a 
•chronic  valvular  lesion. 

Ulcerative  Endocarditis. — Under  this  head  are  reckoned  those 
•cases  of  inflammation  of  the  endocardium  which  manifest  more 
or  less  pronounced  symptoms  of  general  sepsis,  whether  the  ter- 
mination is  in  death,  by  far  the  more  frequent  occurrence,  or  in 
recovery,  of  which  instances  are  now  and  then  reported.  As 
might  be  expected  from  a  consideration  of  the  etiology  and  mor- 
bid anatomy  of  this  class  of  cases,  the  clinical  picture  varies  much, 
according  as  the  local — that  is,  cardiac — or  the  general  symptoms 


164  DISEASES  OF  THE  HEART 

predominate.  In  the  majority  of  cases  the  symptoms  are  those  of 
general  sepsis,  with  very  subordinate,  or  it  may  be  with  no  mani- 
festations on  the  part  of  the  heart.  In  such  cases  the  inflamma- 
tory chaniies  in  the  endocardium  are  to  be  regarded  as  merely  an 
incident  of  the  general  infection,  and  therefore  Rosenbach  classi- 
fies these  cases  as  merely  local  manifestations  of  a  general  infec- 
tion. The  endocarditis  is  but  one  of  the  many  possible  local  ex- 
pressions of  the  infection,  in  consequence  of  the  profound  disturb- 
ance of  nutrition  there  induced. 

In  this  class  of  cases  the  conspicuous  features  are  phenomena 
characteristic  of  pyaemia,  an  irregularly  continuous  pyrexia,  with 
few  if  any  rigors,  sweatings,  great  prostration,  anannia,  emacia- 
tion, anorexia,  diarrhoea,  a  dry,  brownish  tongue,  abdominal  dis- 
tention, stupor  or  low  muttering  delirium,  persistent  dorsal  decu- 
bitus, and  enlargement  of  the  spleen.  The  pulse  is  only  moder- 
ately accelerated,  in  most  instances  impressing  one  as  being  chiefly 
remarkable  for  its  feebleness  and  want  of  tension,  Avhile  the  heart 
may  display  absolutely  no  evidence  of  disease,  or  may  be  slightly 
<lilated,  with  a  faint,  soft  systolic  apex  or  basic  murmur,  the  same 
as  in  typhoid  fever.  Indeed,  this  whole  condition  is  so  like  enteric 
fever  as  to  be  frequently,  it  may  be  said  usually,  mistaken  for 
that  disease. 

In  other  cases  the  fever  is  much  less  typically  sci)tic,  remit- 
ting or  intermitting,  not  dropping  suddenly  below  normal,  and 
again  abruptly  shooting  up  several  degrees,  but  running  so  mild 
a  course  as  to  scarcely  merit  the  appellation  of  pyrexia. 

In  others,  again,  the  elevation  of  temperature  is  of  irregular 
type,  or  there  are  diurnal  fluctuations,  to  possibly  101.5°  or  even 
102.5°  F.  The  feature  that  mainly  attracts  attention  in  such 
cases  is  the  progressive  anaemia,  and  the  trifling  changes  discov- 
ered in  the  heart  are  commensurate  with  those  of  amemia. 

The  last  of  July,  1900,  I  was  consulted  by  a  German,  aged 
fifty-eight,  who  was  a  mercliant  in  the  interior  of  Indiana.  His 
family  history  was  unimportant,  and  his  personal  anamnesis  was 
meagre.  He  had  ahvays  considered  himself  well  until  about  a 
year  previously,  when  he  had  suffered  from  bronchitis,  for  which 
he  had  received  medical  treatment,  at  which  time  a  heart-murmur 
was  discovered.  In  ^larch,  1000,  he  had  been  troubled  with 
night-sweats  that   had  resisted  treatment  by  belladonna.      Since 


ACUTE   ENDOCARDITIS 


165 


Fig.  30. — Apex-beat  and  Relative  Cardiac 
DULNESS  (p.  164). 


that  time  he  had  been  losing  ground,  and  altogether  his  weight 
had  decdined  from  ISO  to  137  pounds.     He  gave  a  vague  account 

of  some  gastro-intestinal  dis- 
order in  the  spring,  but  could 
not  recall  any  attack  of  pain 
that  might  have  been  an  at- 
tack of  appendicitis,  hepatic 
or  renal  colic.  Xeither  could 
he  remember  any  injury  or 
local  suppurating  process, 
and  he  had  never  had  rheu- 
matism, pneumonia,  gonor- 
rhoea, or  other  infection. 

The  patient  was  tall,  ema- 
ciated, j)ale,  and  of  a  slight 
yellow  hue,  and  his  conjunc- 
tiva? were  faintly  icteric.  The 
radial  arteries  were  thick- 
ened, and  the  pulse,  of  only 
moderate  tension,  was  regular  and  equal,  100  to  the  minute.  A 
feeble  cardiac  impulse  was  diffused  from  epigastrium  to  the  apex- 
beat,  which,  weak  and  accompanied  by  soft  thrill,  was  situated 
in  the  sixth  interspace,  10  cen- 
timetres to  left  of  median 
line.  Relative  cardiac  dulness 
at  the  level  of  the  fifth  costal 
cartilage  extended  from  5  cen- 
timetres to  right  of  the  mid- 


sternal  line  to  14  centimetres 
to  left  of  the  same  (Fig.  30). 
The  first  sound  at  the  apex 
was  obscured  by  a  murmur 
and  the  second  was  impure, 
but  over  right  ventricle  both 
were  more  distinct,  while  at 
the  base  both  were  faint,  the 
second  being  scarcely  audible, 
the  pulmonic  second  the  loud- 
er   of    the    two ;    both    aortic 


Fig.  31. — Area  of  Maximum  Audibility 
(shaded)  and  Transmission  of  Murmur 
IN  Case  (p.  166). 


166  DISEASES  OF  THE   HEART 

tones  were  distinct,  but  feeble  in  the  cervical  arteries.  A  liarsli 
systolic  niurmnr  was  heard  at  the  apex,  and  was  transmitted 
into  the  middle  of  the  axillary  region  and  to  the  median  line 
in  front,  yet  not  above  the  third  interspace  (Fig.  31).  The 
lungs  were  negative  and  the  abdomen  was  flabby,  moderately  tym- 
panitic, not  tender,  while  in  the  location  of  the  gall  bladder  a  soft 
roundish  body  could  be  plainly  made  out.  The  urine  collected 
over  night  and  analyzed  next  day  gave  following  results:  Quan- 
tity, 800  cubic  centimetres;  cloudy,  specific  gravity,  1.015;  reac- 
tion acid ;  colour,  reddish-yellow ;  urea,  1.4  per  cent ;  mucin  pres- 
ent ;  a  slight  trace  of  albumin ;  no  sugar ;  no  bile ;  no  blood ;  2 
granular  and  a  few  hyaline  casts ;  a  few  cylindroids  and  uric-acid 
crystals,  but  no  pus;  not  examined  for  peptone.  The  blood-ex- 
amination on  that  day  showed  haemoglobin,  40  per  cent ;  red  cells 
per  centimetre,  3,666,230,  jDercentage  of  red  cells,  73.3 ;  corpus- 
cle index,  54.4,  and  number  of  leucocytes  per  centimetre,  13,700. 
His  temperature  at  11.15  a.  m.  was  98.4°  F. 

As  there  was  nothing  in  the  examination  thus  far  to  lead  to 
a  suspicion  of  endocarditis,  the  diagnosis  was  made  of  chronic 
arteriosclerosis,  with  chronic  myocarditis  and  an  atheromatous 
mitral  incompetence  and  a  mild  interstitial  nephritis,  anannia. 
The  patient  was  advised  to  go  into  a  hospital,  where  he  could  re- 
ceive treatment  by  rest,  appropriate  diet,  and  medication.  He 
did  as  advise'd,  but  got  chilled  in  driving  to  the  hospital,  and  at 
my  visit  that  same  afternoon  his  temperature  was  found  to  be 
101.8°  F.,  respirations  normal,  and  pulse  only  moderately  accel- 
erated. This  febrile  reaction  was  thought  to  be  the  result  of  his 
chill,  and  fearing  he  might  develop  uraemia  on  account  of  his 
ne])hritis,  he  was  ordered  to  drink  very  freely  of  hot  water,  so  as 
to  promote  elimination.  The  result  was  that  by  6  r.  m.  he  had 
passed  15  ounces  of  urine,  and  his  temperature  was  normal.  Be- 
lieving this  rise  of  temperature  to  have  been  but  a  transient  flurry, 
I  was  surprised  and  disappointed  to  find  that  later  that  same  even- 
ing his  temperature  again  rose  to  101.4°  F.  The  chest  was  then 
gone  over  carefully,  but  with  negative  results,  and  accurate  record 
was  kept  of  the  amount  and  character  of  the  urine,  also  without 
the  discovery  of  anything  of  importance. 

JJuring  the  succeeding  six  days,  as  shoAvn  by  the  annexed 
chart  (Chart  I),  he  had  a  low  morning  temperature  and  a  moder- 


ACUTE  ENDOCARDITIS 


167 


ate     afternoon 
rexia     with 
perspirations, 
no    rigors 


py- 

slight 

but 

and    he 


asserted  that  he  felt 


well, 
tient 
from 
which 


As    the    pa- 
had       come 

a  State  in 
malaria  is 
common,  his  blood 
was  examined  on 
August  1st  for  Plas- 
modia, but  with 
negative  results. 
jSFevertheless  it  was 
decided  to  test  the 
effect  of  quinine, 
and  on  August  2d 
20  grains  w^ere  ex- 
hibited in  the  early 
morning.  On  that 
day  he  had  no  fe- 
ver, but  on  the  next 
day,  without  qui- 
nine, his  tempera- 
ture went  up  as 
usual  to  101.4°  r. 
On  August  4th  15 
grains  kept  it  down 
to  100°  F.,  and  on 
the  5th  to  100.8° 
F., while  on  the  6th, 
without  the  reme- 
dy, the  temperature 
again  reached 
101.8°  F.,  and  with 
20  grains  on  the  7th 
it  did  not  go  over 
99°  F.     On  the  8th, 




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168  DISEASES  OF  THE   HEART 

without  quinine,  his  temperature  was  102.2°  F.,  on  the  9th  a 
degree  lower,  while  5  grains  t.  i.  d.  on  the  10th  kept  fever  down 
to  100.2°  F. 

The  results  thus  obtained  convinced  nie  that  the  quinine  acted 
as  an  antipyretic,  but  that,  in  spite  of  doses  sufficient  to  exert  a 
more  lasting  influence  in  case  the  symptoms  were  due  to  malaria, 
the  fever  reasserting  itself  so  soon  as  the  drug  was  stopped,  there 
was  some  other  cause  at  work.  The  urine  was  now  tested  again 
for  peptone,  and  with  positive  results.  I  therefore  became  satis- 
fied that  the  case  was  one  of  pyaemia.  It  should  also  be  stated 
that  the  blood  had  been  tested  for  the  Widal  reaction,  and  this 
proved  to  be  absent. 

As  the  gall  bladder  had  been  found  enlarged  at  the  first  ex- 
amination, and  was  still  palpable,  it  was  thought  highly  probable 
that  there  might  be  an  empyema  of  this  receptacle  as  the  source  of 
the  infection.  Accordingly  the  patient  was  seen  by  Dr.  Bayard 
Holmes,  who  corroborated  the  gall-bladder  enlargement  and  con- 
curred in  the  opinion  of  a  probalde  empyema.  This  seemed  all 
the  more  likely  to  be  the  focus  of  infection  from  the  fact  that  no 
disease  could  be  discovered  in  the  rectum  or  elsewhere.  A  few 
days  subsequently  Dr.  Holmes  operated  on  the  gall  bladder,  but 
although  it  was  enormously  distended  with  fluid,  this  was  not 
purulent,  the  condition  being  a  catarrh  and  not  an  empyema. 

jSTo  ill  effect  followed  the  operation,  but  the  wound  healed 
very  slowly.  For  a  day  or  two  the  temperature  fell  somewhat,  but 
then  resumed  its  former  characters,  bei)ig  down  nearly  or  quite  to 
normal  in  the  early  part  of  the  day  and  rising  in  the  afternoon 
or  evening  to  between  101°  and  102°  F.  Rigors  were  never 
manifested,'  and  repeated  queries  concerning  chilly  sensations  al- 
ways elicited  a  positive  denial  of  them.  Perspirations  were  also 
absent,  or  at  the  most  amounted  to  no  more  than  a  scarcely  per- 
ceptible moistness  of  the  skin  M^here  covered. 

Week  by  week  the  patient  lost  in  strength  and  flesh,  and  grew 
more  ana'mic  in  appearance,  although  his  ability  to  take  consider- 
able nourishiiK'iit  jxii-sistcd.  lie  also  displayed  slight  apathy,  lying 
flat  in  bed,  and  changing  position  but  seldom.  Pain  was  not  com- 
plained of,  and  in  vain  was  a  daily  search  kept  up  for  signs  of 
embolism.  During  these  weeks  the  pulse  slowly  and  gradually 
became  a  little  more  accelerated,  reaching  11 G  or  thereabout.     Its 


ACUTE   ENDOCARDITIS  169 

striking  feature  was  its  feebleness.  This  want  of  tension,  together 
with  the  growing  weakness  of  tlie  heart-sounds,  induced  nie  to 
administer  strychnine  in  doses  of  -gV  of  a  grain  4  times  daily, 
along  with  5,  and  afterward  7  drops  of  tincture  of  strophanthus 
thrice  daily.  He  was  also  given  moderate  doses  of  wine  and 
whisky. 

It  was  always  difficult,  owing  to  the  rigidity  of  the  chest-wall 
and  the  voluminousness  of  the  lungs,  to  satisfactorily  map  out 
deep-seated  cardiac  dulness,  but  I  became  convinced  that  the 
heart  gradually  increased  somewhat  in  size,  though  no  more  than 
could  be  attributed  to  myasthenia.  Pari  passu  with  the  increas- 
ing feebleness  of  the  heart-sounds  the  systolic  apex-murmur  aug- 
mented in  intensity  and  extent  of  audibility  until  at  length  it 
spread  throughout  the  entire  prsecordium.  It  remained  to  the 
last  a-  rather  harsh  blowing  murmur,  and  no  new  bruits  ever  devel- 
oped. IsTeither  did  oedema  become  more  than  a  Very  slight  pitting 
over  the  tibise,  and  I  could  not  make  out  any  increase  in  the  size 
of  the  liver  or  more  than  a  trifling  increase  in  the  area  of  splenic 
dulness,  the  organ  not  being  distinctly  palpable. 

In  brief,  the  entire  clinical  history  was  that  of  an  ever-growing 
anaemia,  or  better,  marasmus  with  moderate  intermittent  pyrexia. 
In  this  respect  I  should  think  it  a  fair  example  of  the  type  of 
cases  described  by  Komberg  as  antemic  rather  than  markedly  sep- 
tic, and  yet  there  was  no  doubt  of  the  existence  of  a  mild  pyaemia. 
Peptone  was  repeatedly  found  in  the  urine,  and  thus,  with  the  in- 
creased leucocytosis,  confirmed  the  conclusion  drawn  from  the  tem- 
perature record.  This  is  well  shown  by  the  annexed  chart.  Death 
occurred  the  middle  of  September,  about  eight  weeks  after  he 
came  under  observation,  ]^o  autopsy  was  had,  but  I  believe  this 
Avas  a  pyemia,  with  implication  of  the  endocardium  as  a  secondary 
and  not  a  primary  event. 

In  still  other  cases  of  ulcerative  endocarditis  there  are  rigors, 
sudden  high  elevations  of  temperature,  and  profuse  sweating,  fol- 
lowed by  sharp  decline  of  the  pyrexia,  the  picture  not  unlike  the 
paroxysms  of  malaria,  excepting  that  the  septic  phenomena  lack 
the  periodicity  of  malarial  infection.  Murchison  has  narrated  an 
instance  of  this  kind  that  lasted  three  months,  and  was  so  sug- 
gestive of  malaria  to  the  friends  that  in  deference  to  their  wishes 
quinine  was  freely  administered,  but  without  appreciable  effect  on 
13 


170  DISEASES  OF  THE  HEART 

the  disease.  In  his  case,  however,  there  was  physical  evidence  of 
an  aortic  valvuhir  lesion. 

There  are  other  cases,  again,  in  which  the  temperature  pursues 
a  still  more  erratic  course,  rising  and  falling  abruptly  for  days, 
and  then  suddenly  sinking  to  normal,  or  it  may  be  to  below  normal. 
Remaining  thus  for  days  or  even  weeks,  it  again  assumes  its  for- 
mer irregularly  intermittent  type.  During  the  apyrexial  period 
the  pulse  still  remains  conspicuously  feeble,  and  the  patient  fails 
to  regain  strength,  so  that  by  these  symptoms  it  becomes  manifest 
that  actual  improvement  is  not  taking  place. 

Thus,  whatever  the  various  manifestations,  they  are  in  them- 
selves indicative  of  sepsis,  and  there  is  nothing  to  show  that  the 
heart  has  become  affected.  Occasionally,  on  the  other  hand,  the 
involvement  of  the  endocardium  is  evinced  by  the  appearance  of 
cutaneous  infarcts  or  by  phenomena  of  embolic  plugging  of  vessels 
in  the  intestinal  organs.  The  lodgment  of  emboli  in  the  skin  is 
shown  by  the  appearance  on  the  extremities  or  trunk,  still  more 
rarely  upon  the  neck  and  face,  of  reddish  spots  of  variable  size, 
from  that  of  a  pin's  head  to  a  pea,  or  somewhat  larger.  These 
petechia)  may  be  few  and  scattered  irregularly,  or  they  may  come 
in  showers  and  at  irregular  intervals.  Septic  infarcts  in  the 
liver,  spleen,  kidneys,  etc.,  are  productive  of  abscesses,  which  may 
be  miliary  and  escape  detection  during  life  or  be  of  recognisable 
size.  In  some  instances  the  clinical  picture  is  dominated  by  these 
embolic  phenomena. 

I  recall  a  case  in  which  it  was  the  detection  of  a  splenic  abscess 
which  seemed  to  justify  the  diagnosis  of  septic  endocarditis.  I 
was  asked  by  Dr.  Haskin,  of  Highland  Park,  to  see  a  gentleman 
of  about  sixty  who  had  been  having  irregular  chills,  fever,  and 
sweatings  suggestive  of  malaria.  His  illness  had  begun  six  weeks 
before  with  malaise,  and  had  speedily  developed  the  symptoms 
of  sepsis.  Three  days  prior  to  my  visit  he  had  suddenly  com- 
plained of  sharp  pain  in  the  left  liypochondrium  with  tenderness. 
1  found  him  unconscious,  and  lying  turned  to  the  left  side,  with 
his  thighs  flexed,  skin  hot  and  moist,  pulse  moderately  rapid,  but 
notably  weak  and  soft.  There  was  a  distinct  blowing  systolic 
murmur  in  tlie  mitral  area.  Splenic  dulness  was  greatly  in- 
creased, and  although  palpation  evidently  caused  pain  and  was 
resisted,  a  rather  soft  tumour  having  the  form  of  the  spleen  could 


ACUTE  ENDOCARDITIS  171 

be  felt  extending  well  down  below  the  left  costal  margin.  The 
case  was  thought  to  be  an  instance  of  abscess  of  the  spleen,  prob- 
ably secondary  to  acute  ulcerative  endocarditis.  Death  took  place 
a  day  or  two  later,  and,  although  an  autopsy  could  not  be  ob- 
tained, permission  was  granted  to  make  an  abdominal  incision  for 
the  purpose  of  verifying  the  existence  of  the  abscess.  The  abdo- 
men was  opened  accordingly,  and  so  soon  as  the  doctor's  finger 
pressed  ui^on  the  spleen  the  organ  burst  and  pus  welled  up  over 
his  finger.  In  this  case  no  etiological  factor  could  be  obtained, 
and  yet  it  seemed  plainly  one  of  septic  endocarditis  with  infective 
infarct  in  the  spleen. 

When  emboli  of  this  character  lodge  in  the  kidney,  they  are 
declared  by  albumin,  pus,  and  blood,  with  casts  in  the  urine. 
There  is  a  class  of  cases  characterized  by  Romberg  as  atypical 
which  run  their  course  with  all  appearance  of  an  acute  ha?mor- 
rhagic  nephritis,  albuminuria,  pus,  blood  in  varying  amounts, 
casts,  renal  epithelium,  and  cylindroids. 

This  condition  of  the  urine  persists  throughout,  but  with  re- 
missions and  exacerbations.  A  mildly  irregular,  continuous  fever 
accompanies  the  nephritis,  and  the  patient  displays  pronounced 
and  increasing  anaemia.  It  is  this  feature,  together  with  the  per- 
sistent pyrexia  out  of  proportion  to  the  temperature  usually  ob- 
served in  nephritis,  which  throws  light  on  the  nature  of  the  case. 
The  discovery  of  an  old-standing  valvular  lesion  contributes  great- 
ly to  the  establishment  of  the  diagnosis. 

Lastly,  cases  are  encountered  which  display  such  manifest  car- 
diac symptoms  that  by  some  clinicians  they  are  classed  in  a  special 
group.  These  are  such  as  either  develop  upon  a  chronic  valve- 
lesion  or  occasion  such  rapid  ulceration  and  destruction  of  the 
valves  that  objective  cardiac  phenomena  become  apparent.  Symp- 
toms of  general  sepsis  may  not  be  marked,  or  if  pronounced,  de- 
pend largely  upon  infective  emboli.  The  pulse  is  peculiarly  soft, 
regular  or  irregular,  and  more  or  less  accelerated  out  of  propor- 
tion to  the  degree  of  fever.  The  patient  usually  manifests  djsj)- 
noea,  and  it  may  be  cyanosis.  Both  liver  and  spleen  are  enlarged 
from  congestion  or  infarcts.  Exceptionally  one  may  upon  re- 
peated examinations  of  the  heart  detect  some  evidence  of  changes 
going  on,  such  as  increasing  feebleness  of  impulse,  slight  increase 
in  the  area  of  dulness,  and  perchance  a  soft  murmur  where  previ- 


172  DISEASES   OP  THE     HEART 

oiislj  none  existed,  or  an  alteration  of  one  already  present.  ]More 
often  such  examinations  are  futile,  and  the  diagnosis  is  largely 
conjectural  or  has  to  be  made  from  the  symptom-complex. 

Course  and  Termination. — The  duration  of  acute  ulcera- 
tive endocarditis  is  exceedingly  variable.  The  disease  may  run 
its  course  to  a  fatal  termination  within  a  few  days  from  its  com- 
ing under  observation,  or  its  course  may  be  dragged  out  over  a 
period  of  weeks  and  even  months.  Some  cases  progress  steadily 
to  a  fatal  issue,  while  others  show  periods  of  seeming  improve- 
ment, followed  by  exacerbations  and  more  rapid  decline.  When 
death  is  the  result  it  occurs  either  in  consequence  of  local  changes 
in  the  heart  and  cardiac  asthenia,  or  as  a  result  of  acute  pulmo- 
nary oedema  or  pulmonary  infarcts.  In  other  cases  the  patient  is 
worn  out  by  prolonged  sepsis,  or  death  is  directly  attributable  to 
the  effects  of  embolism  in  the  brain,  kidneys,  spleen^  etc. 

A  gentleman  of  about  forty,  who  had  a  perfectly  compensated 
mitral  regurgitation  of  rheumatic  origin,  became  ill  in  the  fore 
part  of  February  with  what,  from  the  history,  appears  to  have 
been  an  acute  follicular  tonsillitis.  It  subsided  in  a  few  days,  but 
the  man  did  not  regain  his  accustomed  health.  lie  felt  weak  and 
slightly  feverish,  had  vague  pains,  dull  headache,  and  lost  appe- 
tite. Thinking  his  liver  was  at  fault,  he  went  to  French  Lick 
Springs,  Indiana,  and  there  drank  the  waters,  took  a  course  of 
baths,  and  exercised,  but  without  improvement.  While  there  he 
was  annoyed  by  tenderness  and  ])ain  in  the  ends  of  his  fingers, 
and  observed  that  at  such  times  there  was  a  faint  reddish  colour  of 
the  skin  immediately  above  the  roots  of  the  nails.  He  was  told  it 
was  rheumatic. 

At  lengtli,  failing  to  regain  health,  he  returned  home,  and 
towards  the  end  of  A])ril  sought  my  o])inion,  partly  on  account  of 
a  frequent  dry  cough  that  had  recently  develo])ed.  I  had  known 
liiiii  in  liciilth,  and  had  previously  examined  his  heart.  The 
change  in  his  appearance  and  general  condition  shocked  me.  Ilis 
voice  was  weak  and  tremulous,  his  hands  shook,  his  face  was  pale 
and  sallow.  His  eyes  were  not  perfectly  clear,  the  skin  of  his 
arms  and  trunk  was  flabby,  faintly  yellow,  and  altliough  at  first 
dry,  became  bedewed  with  nK)isture  upon  the  exertion  of  undress- 
ing. Ilis  temperature  in  the  mouth  was  90.8°  F.,  and  the  pulse 
of  105  was  weak  and  small,  but  regular.     I  was  struck  by  the  fact 


ACUTE  ENDOCARDITIS 


173 


that  its  rate  did  not  fall 
appreciably,  even  while 
he  was  resting  on  the 
lounge  after  my  exami- 
nation. The  heart  did 
not  seem  to  be  enlarged, 
but  the  apex-beat  was 
feeble  and  preceded  by  a 
short,  scarcely  percepti- 
ble thrill. 

The  old  mitral  sys- 
tolic murmur  was  pres- 
ent, but  in  addition  the 
first  sound  had  a  sugges- 
tion of  a  presystolic 
bruit,  and  the  second 
sound  was  feeble.  The 
lungs  were  negative,  the 
liver  barely  j)alpable,  and 
urine  contained  a  trace  of 
albumin  with  granular 
and  hyaline  casts. 

From  the  history  of 
tonsillitis  and  the  symp- 
toms, I  at  once  suspected 
endocarditis,  and  sent 
him  home  to  bed.  His 
temperature,  which  was 
carefully  recorded  four 
times  daily,  showed  a 
fairly  continuous  py- 
rexia, from  about  100° 
F.  to  101°  F.  and  a  frac- 
tion (Chart  II).  His 
pulse  remained  persist- 
ently in  the  neighbour- 
hood of  105,  and  the 
heart-findings     were     un- 


changed. 


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174  DISEASES  OF  THE   HEART 

strychnine  and  jeast-nnclein  in  full  doses.  The  diet  was  as 
hearty  as  his  feeble  digestion  would  pennit.  He  felt  so  com- 
fortable that  he  Avas  kept  in  bed  with  difficulty.  Things  remained 
in  this  condition  for  two  weeks,  when  he  one  day  complained  of 
localized  pain  and  stiffness  in  the  calf  of  the  left  leg,  but  with  no 
objective  phenomena. 

His  cough  was  so  persistent  that  repeated  examinations  of  the 
lungs  were  made,  at  first  with  negative  results.  At  length  I  dis- 
covered moderate  dulness  of  the  right  upper  lobe  with  ill-defined 
bronchial  breathing,  but  no  rales.  About  this  same  time  enlarge- 
ment of  the  spleen  became  demonstrable.  At  a  loss  to  account  for 
the  changes  at  the  right  apex,  I  requested  Dr.  Arthur  R.  Edwards 
to  see  the  patient.  He  agreed  in  the  view  that  there  was  probably 
septicaemia  with  endocarditis,  but  could  not  give  a  satisfactory  ex- 
planation of  the  pathological  condition  in  the  lung.  The  pain  in 
the  left  leg  he  thought  was  due  to  embolism.  The  faint  blush  at 
the  root  of  the  nails  with  tenderness,  pain,  and  moderate  clubbing 
was  also  observed  by  him,  but  without  special  comment. 

Coincidently  with  the  appearance  of  distinct  signs  in  the  right 
apex  the  fever  rose  a  degree  or  two,  headache  was  complained  of, 
and  cough  without  expectoration  became  troublesome.  This  con- 
dition, which  I  now  believe  was  a  pneumonia  of  the  same  bacterial 
origin  as  the  general  sepsis,  persisted  for  about  two  weeks,  and 
then  gradually  disappeared,  the  lung  clearing  up,  and  the  patient's 
general  condition  returning  to  what  it  was  before  this  attack. 

For  the  next  month  or  six  weeks  the  clinical  picture  remained 
nearly  in  statu  quo.  Occasionally  he  spoke  of  sudden  pains  in 
the  shoulder  or  elsewhere,  which  lasted  for  a  few  days  and  then 
vanished.  Once  he  complained  of  pain  and  tenderness  of  the  liver, 
and  the  organ  became  slightly  more  enlarged.  This  condition  per- 
sisted for  perhaps  a  week,  and  then  disappeared  slowly.  All  this 
time  there  was  the  same  relentless  pyrexia,  which  at  times  fluc- 
tuated rather  more  than  before — but  with  exception  of  its  becom- 
ing somewhat  weaker  in  action  and  sounds,  the  heart  showed  no 
distinct  change. 

The  character  of  the  temperature  is  shown  in  the  annexed 
chart.  Crede's  ointment  was  rubbed  into  the  skin  freely  for  two 
weeks,  and  was  then  succeeded  by  daily  injections  beneath  the  in- 
tegument of  an  old  antistreptococcus  serum  in  doses  of  10  cubic 


ACUTE  ENDOCARDITIS  175 

centimetres.  Although  kej)t  up  for  more  than  a  week  this  treat- 
ment produced  no  results,  unless  perhaps  a  feeling  of  somewhat 
greater  strength  and  a  slight  reduction  of  temperature. 

At  length,  near  the  middle  of  July,  the  patient,  who  all  the 
time  declared  he  did  not  feel  very  ill,  suddenly  experienced  an 
excruciating  j)ain  in  the  third  finger  of  the  left  hand.  The  finger 
became  cold,  pale,  and  exquisitely  sensitive  to  touch,  as  well  as 
so  painful  that  it  prevented  sleep.  Examination  made  it  apparent 
that  an  embolus  had  lodged  in  the  artery  near  the  middle  of  the 
third  phalanx.  Plugging  was  so  complete  and  the  patient's  suf- 
fering so  intense  that  it  became  necessary  to  amputate  the  finger 
on  the  fourth  day.  It  was  now  apparent  that  he  was  failing  stead- 
ily, although  slowly.  The  heart-rate  increased  to  120,  the  apex- 
impulse  less  defined,  the  first  sound  inaudible,  but  the  murmur 
not  appreciably  more  distinct,  indeed  rather  less  intense,  and 
the  fever  increased,  but  without  rigors  or  sweatings.  Indeed, 
throughout  the  illness  these  had  been  conspicuous  by  their  absence. 

I  saw  him  for  the  last  time  on  the  afternoon  of  July  2 2d,  at 
which  time  he  declared  he  felt  so  comfortable  and  happy  that  he 
believed  he  was  going  to  get  well.  His  countenance  was  slightly 
suffused,  and  as  he  had  not  emaciated  greatly,  his  friends  could 
not  realize  how  ill  he  in  reality  was.  -  During  the  forenoon  of  the 
2-ith  he  was  suddenly  seized  with  pain  in  the  lungs,  which  was 
followed  by  violent  coughing  and  the  expectoration  of  blood.  Evi- 
dently pulmonary  infarcts  had  taken  place  and  betokened  the  near 
approach  of  the  end.  The  cough  grew  so  incessant  as  to  require 
considerable  doses  of  morphine  hypodermically  for  its  control. 
These  were  followed  by  unconsciousness,  in  which  condition  he 
lingered  until  the  afternoon  of  Julv  25th,  when  he  suddenlv 
expired. 

The  course  of  this  undoubted  case  of  septic  endocarditis  occu- 
pied five  months  from  the  attack  of  tonsillitis.  It  was  plainly  one 
of  sepsis  from  the  date  of  his  visit  to  my  office,  yet  without  the 
occurrence  of  embolisms  there  was  little  to  direct  one's  attention 
to  the  heart.  I  was  familiar  with  the  previous  condition  of  the 
heart,  and  hence  able  to  detect  slight  alteration  in  the  physical 
signs  which  might  have  been  otherwise  unrecognised.  Yet  the 
thina;  that  riveted  mv  attention  from  the  start  was  the  almost  un- 
swerving  persistence  of  the  pulse  at  very  nearly  the  same  rate, 


176  DISEASES  OP  THE   HEART 

105,  in  spite  of  rest  in  bed,  until  near  the  termination  of  the  case, 
when  it  rose  to  120. 

A  highly  interesting  feature  also  was  the  condition  of  the  ter- 
minal phalanges  of  the  fingers.  The  faint  redness,  pain,  and,  it 
seemed  to  me,  slight  increase  of  heat,  were  due  to  capillary  dilata- 
tion, which  caused  the  ends  of  the  fingers  to  become  distinctly 
bulbous  in  the  course  of  a  few  months.  During  the  preceding 
winter  I  had  observed  this  same  phenomenon,  only  to  a  much 
more  marked  extent,  in  a  young  woman  who  was  in  the  ward  at 
Cook  County  Hospital  suffering  from  mitral  disease,  and,  judging 
from  the  symptoms,  from  endocarditis.  She  subsequently  left  the 
hospital,  so  that  I  cannot  state  the  cardiac  condition  definitely. 
In  her  case  the  finger-ends  became  distinctly  red  and  unmistak- 
ably bulbous.  In  both  these  instances  there  was  pyrexia  associ- 
ated with  cardiac  disease.  May  not  this  phenomenon  in  the  finger- 
tips point  to  something  more  than  mere  capillary  paresis,  perhaps 
to  such  a  disturbance  of  the  cardio-vascular  apparatus  as  may  sug- 
gest involvement  of  the  heart  as  well  as  general  infection  ?  It  is 
a  matter  of  profound  regret  that  an  autopsy  could  not  be  obtained 
in  the  case  which  has  been  narrated  at  such  length. 

Physical  Signs. — Inspection  is  of  very  negative  value,  since 
although  it  may  enable  one  to  detect  signs  of  circulatory  disturb- 
ance, it  does  not  furnish  proof  of  such  disturbance  being  due  to 
endocarditis.  Besides,  valvulitis  is  so  often  masked  by  the  symp- 
toms and  physical  signs  of  the  primary  affection  that  inspection 
of  the  patient  reveals  only  such  changes  in  the  patient's  appear- 
ance as  belong  to  the  rheumatism  or  other  original  disease. 

Palpaiion  is  likewise  of  minor  aid  in  \]u)  detection  of  acute 
endocarditis.  It  may  assist  in  the  recognition  of  some  old-stand- 
ing valvular  lesion,  or  in  determining  the  presence  of  abnormal 
pulsations,  variations  in  the  force,  position,  and  extent  of  the 
apex-boat,  the  possible  development  of  tlirills  in  the  course  of  the 
affection,  enlargement  or  not  of  the  liver,  etc.,  all  findings  that 
bear  in  certain  cases  on  the  condition  of  the  heart,  but,  lik(^  inspec- 
tion, it  cannot  furnish  direct  evidence  of  tlie  existence  of  acute 
endocarditis.  Its  chief  value  is  in  the  diidy  of  the  pulse,  which 
in  all  suspected  cases  should  be  carefully  studied,  changes  in  its 
tension  being  often  of  greater  value  than  alterations  of  rate  or 
rhytvlmi. 


ACUTE  ENDOCARDITIS  177 

Percussion. — This  is  indispensable  if  one  will  correctly  appre- 
ciate the  significance  of  anscnltatory  phenomena,  since  the  condi- 
tion which  occasions  an  organic  murmur  also  leads  to  dilatation 
or  hypertrophy,  and  therefore  to  a  corresponding  alteration  in  the 
area  of  cardiac  dulness.  If  endocarditis  occasions  mitral  incom- 
petence, it  will  also  eventually  occasion  secondary  enlargement  of 
the  right  ventricle.  Consequently  daily  percussion  over  this  cham- 
ber should  be  made  in  order  to  detect  the  earliest  ej^^idence  of  any 
alteration  in  the  outline  of  the  right  and  lower  cardiac  border. 
On  the  other  hand,  aortic  disease  produces  increase  of  dulness  on 
the  left  side  with  gradual  alteration  in  the  position  of  the  apex- 
beat.  Accordingly  percussion  is  of  very  great  value,  since  without 
the  information  derived  from  it  a  careful  diagnostician  would 
scarcely  venture  on  an  opinion  concerning  the  nature  of  an  endo- 
cardial murmur,  especially  an  apex-murmur,  which,  as  is  well 
known,  is  of  frequent  occurrence  in  febrile  affections  without 
inflammatory  changes  in  the  valves. 

Auscultation. — Even  this  furnishes  only  exceptionally  a  trust- 
worthy means  of  recognising  endocarditis,  for,  as  will  be  sho^vn 
later  on,  a  murmur  is  not  always  to  be  accepted  as  an  indication 
of  valvulitis. 

It  is  not  so  much  the  detection  of  an  actual  murmur  that  is 
significant,  as  it  is  the  recognition  of  changes  in  the  character 
and  relative  intensity  of  the  cardiac  tones.  Daily  careful  study  of 
the  sounds  must  be  made  therefore.  The  earliest  evidence  that  all 
is  not  right  at  the  mitral  orifice  (the  seat  of  inflammation  in  50 
per  cent  of  cases)  is  said  by  English  observers,  who  it  must  be 
acknowledged  have  given  close  attention  to  this  subject,  to  be  not 
a  murmur,  but  a  muffling  or  indistinctness  of  the  first  sound  at  the 
apex.  A  blowing  murmur,  which  is  purely  accidental,  may  ac- 
company the  first  sound  in  a  given  case,  and  hence  the  occur- 
rence of  a  murmur  with  the  sound  is  not  so  significant  as  an  alter- 
ation in  the  sound  itself,  since  it  is  reasonable  to  assimie  that  if  the 
production  of  the  soimd  is  interfered  with  it  may  be  by  inflam- 
matory changes.  Such  alteration  of  the  second  sound  at  the  base 
is  likewise  suspicious  of  endocarditis  affecting  the  semilunar 
valves. 

If  in  a  case  impurity  of  any  of  the  tones  is  observed,  it  is  very 
likely  to  grow  into  a  more  or  less  distinct  murmur  in  the  course 


178  DISEASES  OF  THE   HEART 

of  time,  Avliile  there  will  also  develop  the  secondary  changes  in  the 
heart  approi)riate  to  the  lesion,  whatever  it  may  be. 

A  diastolic  murmur  developing  in  the  aortic  area  may  be  set 
down  as  not  accidental,  and  therefore  indicative  of  inflammation 
at  this  ostium.  If  this  inflammation  seriously  impair  the  integrity 
of  the  valve,  it  will  be  shown  in  time  by  the  occurrence  of  the 
secondary  cardiac  and  vascular  signs,  which  are  described  at 
length  in  the  chapter  on  Aortic  Regurgitation. 

A  presystolic  murmur  rarely  develops  as  a  result  of  acute  endo- 
carditis unless  the  process  is  ingrafted  upon  an  old-standing  mitral 
regurgitation.  Inflammation  attacking  previously  healthy  valves 
usually  produces  incompetence  of  these,  or  this  combined  with  a 
minor  degree  of  obstruction.  Therefore,  the  murmur  is  apt  to  be 
purely  systolic,  or  systolic  with  a  very  short,  scarcely  recognisable 
presystolic  one.  When,  however,  an  old  endocarditis  affecting  the 
mitral  valve  becomes  rekindled,  as  not  infrequently  happens,  then 
a  presystolic  bruit  may  develop,  and  so  developing  it  furnishes 
almost  indubitable  proof  of  endocarditis  being  present.  This  cir- 
cumstance has  more  than  once  enabled  me  to  diagnosticate  correctly 
the  occurrence  of  endocarditis,  as  proved  by  subsequent  events. 

A  systolic  murmur  in  any  of  the  cardiac  areas  must  always  be 
regarded  with  doubt  until  its  true  significance  is  shown  by  the 
development  of  secondary  physical  signs.  This  is  true  of  such  a 
murmur  even  in  the  aortic  notch,  for  experience  has  taught 
that  even  here  a  murmur  may  be  accidental.  It  is,  however,  in  the 
case  of  an  apex  systolic  murmur  ])articularly  that  caution  must 
be  exercised.  (1)  Because  accidental  bruits  are  most  often  mitral, 
or  mitral  and  pulmonic.  (2)  Because  such  a  mitral  systolic  mur- 
mur may  be  the  result  of  a  previously  existing  regurgitation,  and 
not  at  all  due  to  the  rheumatism  in  the  course  of  which  it  may 
happen  to  be  discovered.  (3)  Because,  as  shown  by  a  case  re- 
ported by  James  W.  Walker,  of  this  city,  an  endocarditis  nuiy 
exist  without  its  giving  rise  to  any  murmur  whatever.  In  his 
case  the  anterior  and  left  posterior  aortic  cusps  presented  on  their 
surface  large  masses  of  soft,  friable,  nodular  vegetations,  which 
had  filled  the  ostium,  and  yet  repeated  and  careful  examinations 
during  life  liad  utterly  failed  to  detect  any  murmur. 

Diagnosis. — These  three  considerations  make  very  plain  the 
fallacy  of  depending  upon  the  2)resence  or  absence  of  a  murmur 


ACUTE  ENDOCARDITIS  179 

in  making  a  diagnosis  of  acute  endocarditis.  Inasmuch,  therefore, 
as  acute  simple  endocarditis  may  escape  detection  entirely  or  may 
be  only  suspected,  one  is  frequently  compelled  to  leave  its  diag- 
nosis an  open  question  until  after  it  has  occasioned  sufficient 
structural  change  to  produce  secondary  physical  signs.  One  must 
.  therefore  depend  upon  the  history  and  symptoms  even  more  than 
on  distinctive  objective  signs. 

Even  the  pyrexia,  acceleration  of  the  pulse  and  respiration, 
prjipcordial  pain,  nervousness,  and  restlessness  may  all  be  attribu- 
table to  the  rheumatism.  When  the  endocarditis  is  mural — i.  e., 
confined  to  the  lining  membrane  of  the  cavities — the  valves  escap- 
ing altogether,  a  positive  diagnosis  cannot  be  made  without  the 
occurrence  of  embolic  phenomena. 

Differential  Diagnosis. — Acute  pericarditis  is  scarcely  likely 
to  be  mistaken  for  acute  simple  endocarditis,  and  yet  it  is  con- 
ceivable that  such  might  be  the  case  when  the  friction-murmur 
happens  to  coincide  with  one  of  the  heart-sounds,  and  hence  simu- 
late an  endocardial  bruit.  In  such  a  case  the  greater  pain  and 
the  subsequent  development  of  signs  of  effusion  ought  to  set  one 
right.  Should  an  inexperienced  auscultator  mistake  a  to-and-fro 
pericardial  rub  over  the  base  of  the  aorta  for  the  double  murmur 
of  aortic  insufficiency  of  recent  origin,  he  may  be  able  to  correctly 
interpret  the  rub  by  noting  the  absence  of  the  secondary  cardiac 
and  vascular  signs  of  an  aortic  valve-lesion. 

Pernicious  ancemia  may  under  some  circumstances  very  closely 
simulate  acute  endocarditis  without  embolic  phenomena.  I  have 
seen  such  a  case,  in  which  the  systolic  apex-murmur  of  ever-in- 
creasing intensity,  the  low  irregular  pyrexia,  great  prostration, 
pain  in  the  hepatic  region,  with  nausea  and  vomiting,  were,  to- 
gether with  a  history  of  infection  of  the  forefinger  and  lymphan- 
gitis four  months  earlier,  highly  suggestive  of  a  low  grade  of  en- 
docardial inflammation,  particularly  as  the  patient  gave  additional 
history  of  rheumatism.  The  blood-examination  and  ultimate  au- 
topsy findings  established  the  correct  diagnosis. 

The  Diagnosis  of  Ulcerative  Endocarditis  may  in  some  cases  be 
easy,  in  others  only  a  matter  of  conjecture.  What  has  been  said 
concerning  the  physical  signs  of  the  simple  applies  equally  well 
to  the  malignant  form.  In  some  instances  the  entire  clinical  pic- 
ture is  that  of  general  sepsis,  and  there  are  no  findings  to  betray 


180  DISEASES  OF   THE   HEART 

its  localization  in  the  heart.  Tii  otlicrs  characteristic  signs  of 
valvular  insufficiency  develop  or  the  tokens  of  an  old  lesion  un- 
dergo modification,  or  indications  of  a  new  lesion  become  added 
to  those  of  a  pre-existing  defect.  For  these  reasons  repeated  and 
minute  examinations  of  the  lieart  are  necessary.  The  detection 
of  a  murmur  is  in  itself  of  small  moment  sometimes,  Lut  the  dis- 
covery of  changes  in  the  rhythm  of  one  already  existing,  as  by  a 
presystolic  being  prefixed  to  a  systolic  bruit,  or  an  alteration  in  its 
timbre,  a  previously  soft  one  becoming  harsh  or  musical,  or  the 
addition  of  a  diastolic  murmur  to  a  systolic  one,  all  such  modifica- 
tions are  of  great  significance,  and  sh(»uld  be  carefully  noted. 

The  most  reliable  aid  in  the  diagnosis  of  malignant  endocar- 
ditis is  found,  however,  in  the  history  and  symptoms.  One  must 
always  seek  for  an  efficient  etiological  factor.  For  example,  it  was 
not  a  great  while  ago  that  I  was  asked  to  see  in  consultation  a 
young  woman  who  was  running  an  irregular  course  of  fever,  was 
emaciating,  losing  strength,  and  had  a  cardiac  murmur.  It  was 
evident  at  a  glance  that  she  was  suffering  from  pronounced  sep- 
tica-mia,  but  the  question  that  the  physician  wanted  cleared  up 
was  whether  the  cardiac  findings  indicated  septic  endocarditis. 
There  was  history  of  an  old  rheumatic  mitral  disease.  It  did  not 
require  very  long  search  to  find  evidences  of  cutaneous  infarcts, 
and  when  in  response  to  inquiry  concerning  a  vaginal  discharge, 
the  nurse  stated  that  there  had  been  an  extremely  ofi^ensive  one 
earlier  in  the  illness^  and  when  a  vaginal  examination  disclosed 
cervical  laceration,  the  chain  of  testimony  was  complete.  An  abor- 
tion had  led  to  uterine  infection,  this  to  septicaemia,  and  this  lat- 
ter to  an  ulcerative  process  within  the  heart,  which  was  predis- 
posed to  iullaiimuition  by  its  old-standiug  mitral  l(>si(m. 

Symptoms  of  })ya'mia — i.  e.,  chills,  fever,  and  sweating — in- 
dicate general  sepsis,  but  do  not  warrant  the  inference  that  the 
endocardium  is  involved.  This  can  only  be  assumed  when  embolic 
phenomena  are  discovered  or  there  are  some  cardiac  findings  as 
well  as  symptoms  of  general  sepsis.  It  is  very  necessary,  there- 
fore, to  make  (htily  cxaniination  of  the  skin,  spleen,  and  urine  for 
detection  of  the  changes  already  mciitioiicd  as  forming  an  essen- 
tial part  of  the  symptomatology  of  this  form  of  endocarditis. 

In  the  very  obscure  cases  in  which  end)olic  phenomena  are  not 
present  and  there  are  no  cardiac  findings  to  exjdain  the  pyrexia 


ACUTE   ENDOCARDITIS  181 

and  other  features  that  point  to  infection,  yet  in  which  the  feeble- 
ness of  pulse  and  heart-sounds  suggest  the  possibility  of  a  primary 
focus  of  infection  in  the  endocardium,  information  is  likely  to  be 
obtained  from  examination  of  the  blood.  Usually  in  infections 
there  is  pronounced  leucocytosis,  but  in  a  few  cases  Neusser  found 
an  absence  of  increase,  and  he  consequently  concluded  that  when 
in  a  given  case  of  septicaania  there  is  either  an  absence  or  possi- 
bly a  decrease  of  leucocytosis,  it  points  to  the  likelihood  of  ma- 
lignant endocarditis.  Bacteriological  examination  of  the  blood 
in  a  suspected  case  is  not  often  productive  of  results,  and  yet 
should  be  made  when  all  other  means  of  arriving  at  a  diagno- 
sis fail. 

Differential  Diagnosis. — It  is  not  sufficient  to  merely  make  a 
diagnosis  of  acute  endocarditis ;  one  must  also  determine  its  na- 
ture. Therefore  in  making  a  differential  diagnosis  the  following 
points  may  be  of  assistance:  (1)  The  possible  etiological  factor; 
in  the  simple  form,  articular  rheumatism,  chorea,  scarlatina,  or 
some  other  generally  recognised  cause  of  benign  endocarditis ;  in 
the  ulcerative,  some  antecedent  pus  infection  or  focus  of  suppura- 
tion, croupous  pneumonia,  gonorrhcea,  rectal  abscess,  otitis  media, 
quinsy,  trauma,  furuncle,  carbuncle,  leg  ulcer,  etc.  (2)  The  char- 
acter of  the  temperature.  In  simple  endocarditis  fever  may  be 
absent  or  due  to  the  primary  disease,  subsiding  with  the  disap- 
pearance of  the  rheumatism,  etc.,  or  it  may  pursue  a  mild  con- 
tinuous course.  In  the  ulcerative  form  the  temperature-curve  is 
that  of  pus-infection  of  the  characters  that  were  described  in  the 
symptoms.  (3)  Blood  changes  and  bacteriological  examination 
of  the  blood  are  negative  in  the  simple  form,  while  in  the  malignant 
there  may  be  pronoimced  leucocytosis.  The  occurrence  of  septic 
phenomena  without  such  increase  points  to  septic  endocarditis. 

(4)  Urinary  findings.  The  discovery  of  albumin,  pus,  and  blood 
with  casts  is  in  favour  of  mycotic  endocarditis,  since  hsemorrhagic 
nephritis  is  not  a  part  of  the  clinical  history  of  the  simple  form. 

(5)  Hgemorrhages  into  the  skin  or  from  the  mucous  membranes 
may  occur  in  the  ulcerative,  but  not  in  the  benign  variety  of  endo- 
carditis. (6)  Embolic  phenomena,  although  occasionally  observed 
in  the  simple,  are  yet  generally  found  in  the  malignant  endocar- 
ditis. (7)  Enlargement  of  the  spleen  is  in  favour  of  the  mycotic 
as  against  the  simple  form.     (8)  Eecovery  is  the  rule  in  simple 


182  DISEASES  OF  THE  HEART 

and  the  exception  in  ulcerative  endocarditis,  although  its  course  to 
a  fatal  issue  may  be  slow. 

Typhoid  fever  is  the  disease  above  all  others  for  which  ulcer- 
ative endocarditis  is  likely  to  be  mistaken.  As  a  matter  of  fact, 
most  cases  of  the  latter  affection  are  diagnosed  as  enteric  fever, 
and  so  regarded  until  in  the  dead-house  they  are  found  otherwise. 
The  points  of  difference  are  the  following:  (1)  In  typhoid  fever 
the  temperature  is  not  so  erratic,  and  in  the  first  week  often  dis- 
play's the  characteristic  gradiuilly  ascending  curve.  (2)  The  pulse 
in  this  disease  is  usually  slow,  out  of  proportion  to  the  degree  of 
temperature.  In  its  want  of  tension  during  the  height  of  the 
malady  it  may  be  like  that  of  endocarditis.  (3)  Splenic  enlarge- 
ment comes  at  an  earlier  period  in  enteric  fever,  and  is  more  con- 
siderable. (4)  Rose-spots  usually  appear  between  the  eighth  and 
twelfth  day,  are  apt  to  be  in  crops  upon  the  trunk,  disappear 
temporarily  on  pressure,  are  of  a  nearly  uniform  size,  and  have  a 
darker  centre,  fading  out  towards  the  periphery.  Cutaneous  em- 
bolisms, on  the  contrary,  appear  most  often  upon  the  extremities, 
are  irregularly  distributed,  of  variable  size,  do  not  fade  on  pres- 
sure, and  have  a  necrotic  pale  centre,  becoming  of  a  deeper  colour 
towards  the  edge.  (5)  The  stools  of  abdominal  typhus  are  often, 
though  by  no  means  always,  diarrhcfal,  have  the  pea-soup  appear- 
ance, and  contain  the  Ebertli  bacillus.  (6)  Typhoid-fever  pa- 
tients are  very  apt  to  manifest  signs  of  bronchitis.  (7)  Except- 
ing epistaxis  early  in  its  course  and  possible  haimorrhage  from  the 
bowel  during  the  middle  or  latter  portion,  lumnorrhages  are  not 
common  in  typhoid  fever.  (8)  In  the  Widal  agglutination  test 
we  now  possess  a  reliable  means  of  differentiating  enteric  fever 
from  malignant  endocarditis,  and  it  should  invariably  be  made  in 
every  doubtful  case.* 

The  value  of  this  differential  test  was  shown  in  a  case  under 
my  care  a  few  months  ago.  A  young  man  with  extreme  aortic 
regurgitation  of  rheumatic  origin  was  under  treatment  for  attacks 
of  pni'cordial  pain,  and  as  there  were  symptoms  pointing  to  a  rup- 
ture of  compensation  he  was  put  to  bed.  A  few  days  thereafter 
he  began  to  manifest  a  low  grade  of  irregular  temperature,  but 
without  any  other  symptoms.     His  ])ulso  remained  disproportion- 

*  According  to  MacFarland,  there  was  in  4,000  cases  only  4  per  cent  of  error. 


ACUTE   ENDOCARDITIS  183 

ately  slow,  and  I  at  once  suspected  typhoid  fever,  although  not 
unmindful  of  the  possibility  of  endocarditis.  Rose-spots  were 
never  discovered,  notwithstanding  repeated  daily  inspection  of 
the  trunk,  and  splenic  enlargement  could  never  be  satisfactorily 
made  out  either  by  palpation  or  percussion.  There  was  no  diar- 
rhoea at  any  time,  the  bowels  being  rather  confined.  The  Widal 
test  was  resorted  to  at  the  end  of  the  first  week,  and  settled  the 
diagnosis  as  one  of  enteric  fever.  Had  this  means  of  differential 
diagnosis  not  been  available  I  should  have  felt  exceedingly  uneasy 
as  to  the  nature  of  the  case  and  its  possible  outcome.  As  it  was, 
I  felt  no  more  anxiety  than  would  be  natural  in  such  a  severe 
valvular  lesion,  complicated  by  the  occurrence  of  the  abdominal 
typhus,  and  a  possible  infection  of  the  chronic  endocarditis  in  con- 
sequence. 

The  error  of  mistaking  ulcerative  endocarditis  for  malarial 
infection  is  so  easily  avoidable  nowadays  by  the  discovery  of  the 
Plasmodia  that  it  ought  never  to  be  committed,  and  is  inexcusable. 

Prognosis. — This  depends  not  only  upon  the  nature  of  the 
endocarditis,  whether  benign  or  ulcerative,  but  also  upon  certain 
modifying  conditions,  as  the  extent  and  seat  of  the  inflammation, 
the  concurrence  or  not  of  acute  pericarditis  or  myocarditis, 
whether  it  is  a  first  attack  or  has  been  ingrafted  upon  a  chronic 
endocarditis,  and  lastly  upon  the  presence  or  absence  of  septic  in- 
farcts. If  the  inflammation  expend  its  energies  in  a  local  deform- 
ing process  through  the  development  of  new  connective  tissue 
within  the  valves,  or  the  formation  of  vegetations  upon  their  sur- 
face, or  that  of  the  contiguous  orifice,  the  endocarditis  does  not 
usually  destroy  life  directl}'^,  but  leaves  the  individual  with  a  per- 
manent valvular  defect.  This  statement  must  be  modified,  how- 
ever, in  accordance  with  the  seat  of  the  inflammation.  If  this  is 
confined  to  the  left  auriculo-ventricular  opening,  which  fortu- 
nately is  the  case  in  at  least  one-half  of  the  instances,  the  imme- 
diate prognosis  is  much  less  grave  than  when  the  endocarditis 
attacks  the  aortic  valves,  rendering  them  incompetent.  Rapidly 
induced  insufficiency  occasions  dilatation  of  that  chamber  into 
which  the  blood  regurgitates. 

The  secondary  effect  of  endocarditis  of  the  mitral  cusps  is 
dilatation  of  the  left  auricle,  of  the  aortic  cusps,  dilatation  of  the 
left  ventricle,  and  there  is  abundant  proof,  both  clinical  and  other- 


184  DISEASES  OP  THE   HEART 

wise,  that  dilatation  of  the  auricle  is  less  dangerous  to  life  than 
dilatation  of  the  ventricle.  Moreover,  in  mitral  regurgitation,  the 
resistance  offered  by  the  walls  of  the  left  auricle  is  re-enforced 
by  the  column  of  blood  in  the  pulmonary  vessels  and  by  the  right 
ventricle,  while  in  insufficiency  of  the  aortic  valve  there  is  not  only 
danger  of  paralysis  of  the  left  ventricle  from  overdistention,  but 
if  in  consequence  of  stretching  of  this  cavity  and  of  the  left  au- 
riculo-ventricular  ring  the  mitral  valves  become  relatively  incom- 
petent, the  evils  and  dangers  of  mitral  are  added  to  those  of  aortic 
regurgitation. 

If  the  inflammatory  process  extend  also  to  the  myocardium 
or  pericardium  the  prognosis  becomes  far  more  serious,  since  the 
myocarditis  favours  a  rapid  dilatation  of  the  organ.  Sturges 
directed  attention  to  the  liability  in  children  to  inflammation  of 
all  of  these  structures,  giving  it  the  name  "  acute  carditis,"  and 
pointed  out  the  extremely  serious  nature  of  this  condition.  The 
gravity  of  the  prognosis  in  these  cases  is  attested  by  the  following 
figures,  to  which  reference  has  already  been  made  in  the  chapter 
on  Acute  Pericarditis:  Of  150  cases  of  fatal  rheumatic  endocar- 
ditis in  children,  Poynton  found  the  pericardium  healthy  in  only 
9,  while  in  34  the  myocardium  showed  changes  of  one  kind  or  an- 
other. Death  was  thought  attributable  to  the  condition  of  the 
myocardium  rather  than  to  that  of  the  endocardium. 

If  an  acute  endocarditis  becomes  ingrafted  upon  the  chronic 
process,  or  attacks  valves  already  the  seat  of  sclerotic  changes,  the 
prognosis  becomes  very  doubtful,  since  it  is  a  well-known  fact  that 
under  such  circumstances  the  inflammatory  process  is  very  likely 
to  prove  septic.  Moreover,  even  if  the  endocarditis  should  not  be 
malignant,  it  is  certain  to  intensify  the  changes  already  existing, 
either  by  causing  still  greater  destruction  of  the  valves  or  by  trans- 
forming a  predominating  insufficiency  into  a  stenosis  through  the 
development  of  thrombi  about  the  edges  of  the  opening.  Thus  a 
lesion  which  was  compensated  may  be  converted  into  one  of  such 
gravity  that  compensation  is  never  again  possible. 

1'he  occurrence  of  embolisms  renders  the  prognosis  exceed- 
ingly serious,  both  as  tf»  the  immediate  and  remote  effects.  Even 
in  simple  rheumatic  endocarditis  an  eiid)olus  may  be  carried  into 
the  brain,  the  left  middle  cerebral  artery  being  the  one  most  fre- 
quently plugged,  and  occasion  hemiplegia.     In  the  case  of  endo- 


ACUTE  ENDOCARDITIS  185 

carditis  of  the  rigiit  heart,  pnhnonary  infarcts  frequently  con- 
tribute to  the  fatal  termination.  Should  the  emboli  be  septic,  more 
than  a  mechanical  effect  is  produced.  Single  or  multiple  abscesses 
in  the  spleen,  liver,  kidneys,  or  even  scattered  throughout  the 
body,  set  up  symptoms  of  general  infection.  These  are  the  cases 
properly  classed  under  the  category  of  malignant  endocarditis, 
since  in  them  death  is  the  inevitable  result.  Should  the  urine  at 
any  time  display  the  characters  of  ha^morrhagic  nephritis,  it  is  to 
be  regarded  as  an  omen  of  evil  import. 

The  very  interesting  and  practical  question  arises.  Can  acute 
rheumatic  endocarditis  subside,  leaving  the  valves  uninjured  ? 
This  query  has  been  answered  in  the  affirmative  by  some  writers, 
their  belief  being  based  upon  the  disappearance  of  a  systolic  apex- 
murmur  that  had  been  observed  to  develop  during  an  acute  rheu- 
matic attack.  My  experience  has  been  too  limited  to  warrant  miy 
forming  an  opinion  upon  the  subject,  yet  I  frankly  state  I  would 
be  loath  to  accept  any  other  than  post-mortem  evidence  of  the  cor- 
rectness of  such  a  belief.  Under  the  influence  of  infection  and 
pyrexia,  weakening  of  the  myocardium  and  papillary  muscles  may 
very  readily  occasion  dilatation,  and  a  systolic  murmur  in  the 
mitral  area  be  developed.  With  returning  health  these  may  re- 
gain their  tone,  and  the  dilatation  and  murmur  disappear.  Can 
any  one  assert  therefore,  without  fear  of  contradiction,  that  the 
appearance  and  subsequent  disappearance  of  such  physical  signs 
indicate  recovery  from  acute  endocarditis,  and  not  from  cardiac 
dilatation  ?  The  following  case  observed  during  convalescence 
from  pneumonia  is  one  in  point :  A  healthy  young  married  man  of 
twenty-seven  passed  through  a  pneumonia  of  the  right  lower  lobe  in 
the  fall  of  1899.  About  a  week  after  the  crisis,  when  convalescence 
was  progressing  finely,  he  arose  from  bed  early  one  morning  and 
walked  into  the  adjoining  bath-room  to  pass  his  urine.  He  sud- 
denly became  weak  and  dizzy,  and  upon  returning  to  his  bed- 
chamber his  pulse  was  observed  to  be  135  to  the  minute  and  weak. 
Whenever  during  that  day  he  attempted  to  walk  about  the  room 
his  pulse  immediately  arose  in  frequency  and  became  correspond- 
ingly diminished  in  strength.  I  was  asked  to  see  him  that  same 
evening,  and  found  him  reclining  on  the  sofa,  his  pulse  about  100, 
regular,  but  compressible,  the  apex-beat  feeble,  in  the  fifth  left 

interspace  slightly  outside  the  nipple-line. 
14 


186 


DISEASES  OF  THE  HEART 


Relative  cardiac  dulness  was  increased  transversely,  particu- 
larly to  the  left,  reaching  12.5  centimetres  to  the  left  of  the  medi- 
an line.  The  temperature  was  normal,  respirations  tranquil,  and 
the  patient  had  no  sense  of  dyspnoea.  Cardiac  sounds  were  every- 
where audible,  but  the  aortic  second  w^as  weak,  and  accompany- 
ing the  first  sound  at  the  ajiex  was  a  faint  systolic  blowing  mur- 
mur. There  was  no  history  of  previous  attacks  of  rheumatism, 
and  until  the  date  of  his  pneumonia  the  patient  had  indulged  in 
much  athletic  exercise  without  shortness  of  breath  or  palpitation. 
Realizing  the  possibility  of  an  acute  endocarditis  of  pneumococ- 
cus  origin,  I  insisted  upon  absolute  physical  repose,  ordered  light 
diet,  and  a  gentle  saline  aperient. 

On  the  following  day,  the  condition  being  essentially  the  same, 
^  of  a  grain  of  strychnine  sulphate  three  times  a  day  was  or- 
dered. As  the  temperature  remained  normal  and  the  murmur 
had  not  increased,  two  days  later  tincture  of  digitalis  was  cau- 
tiously administered.  Within 
twenty-four  hours  the  left 
ventricle  had  come  down  0.5 
centimetres,  and  upon  the 
digitalis  being  increased,  the 
next  twenty- four  hours  wit- 
nessed a  still  further  diminu- 
tion in  the  extent  of  relative 
cardiac  dulness  to  the  left.  In 
the  course  of  the  next  week 
or  ten  days  the  heart  meas- 
ured but  10  centimetres  to  the 
left  of  the  median  line,  and 
w\is  normal  at  the  right  (Fig. 
32). 

Two  months  subsequently, 
after  the  patient  had  been 
without  medicine  for  several 
weeks,  and  liiid  ri'turned  to  liis  usual  mode  of  life,  the  left  ven- 
tricle measured  but  J>  centimetres,  a  reduction  of  more  than  3 
centimetres  since  the  date  of  my  first  examination.  Was  this  case 
to  be  regarded  as  one  of  acute  endocarditis  following  croupous 
pneumonia?     Certaiidy  not.     It  was  one  of  simple  acute  dilata- 


¥m.  '62. —  DlMlNU'i'lON    <.>F    litLATlVK  CaKUIAO 

Dulness  in  One   Week,  under  Tkeat- 
MENT.     Case  (p.  185;. 


ACUTE   ENDOCARDITIS  187 

tion,  chiefly  of  the  left  ventricle,  res^^lting  primarily  from  asthe- 
nia of  the  heart-muscle  in  consequence  of  the  effect  of  the  toxins 
of  the  pneumococcus. 

Treatment. — Clinical  experience  the  world  over  accords  w^ith 
the  conclusion  naturally  drawn  from  a  consideration  of  the  pathol- 
ogy and  morbid  anatomy  of  acute  endocarditis — viz.,  that  when 
the  process  has  once  become  established,  we  possess  no  means  of 
causing  absorption  of  inflammatory  product  or  restoring  the  endo- 
cardium to  a  healthy  state.  It  should  be  our  aim,  therefore,  to 
prevent  where  we  cannot  cure.  Our  first  duty  is  to  study  the  effi- 
cacy of  prophylactic  measures.  Our  efforts  in  this  direction  should 
not  be  restricted  to  prevention  of  endocarditis,  but  should  first  be 
directed  against  that  disease,  articular  rheumatism,  which  is  so 
largely  responsible  for  inflammation  of  the  cardiac  structures. 
Proper  sanitation  and  attention  to  the  diet,  clothing,  habits,  and 
occupation  of  patients  may  do  much  to  this  end. 

Of  special  value  are  all  measures  calculated  to  maintain  a  high 
standard  of  nutrition,  and  persons  of  distinct  rheumatic  diathesis 
should  be  impressed  with  the  danger  of  exposure  to  wet  and  cold. 
Children  in  whom  rheumatic  manifestations  are  obscure,  should  be 
carefully  examined  whenever  ailing,  for  possible  evidence  of  rheu- 
matic infection,  and  if  this  be  discovered,  should  promptly  be 
given  some  preparation  of  a  salicylic  acid. 

Much  has  been  written  concerning  the  prevention  of  cardiac 
involvement  during  rheumatic  attacks;  and  when  the  salicylic- 
acid  treatment  of  rheumatism  came  into  use,  strong  hope  was 
entertained  of  its  ability  to  prevent  endocarditis.  Even  now  there 
are  those  who  believe  that  by  diminishing  the  severity  of,  or  even 
cutting  short,  the  rheumatic  attack,  this  treatment  lessens  the  lia- 
bility to  cardiac  inflammation.  The  same  also  may  be  said  of  the 
alkaline  treatment,  or  of  the  combinations  of  the  alkalies  and 
salicylates.  For  the  most  part,  observers  of  long  experience  have 
come  to  the  conclusion  that  whereas  the  salicylate-treatment  does 
not  assure  the  prevention  of  endocarditis  it  would  better  be  per- 
severed with,  since  if  properly  administered  it  is  not  likely  to  do 
harm.  For  my  part  I  do  not  believe  in  the  prophylactic  power 
of  this  drug  over  the  cardiac  manifestations  of  articular  rheu- 
matism. 

Given  a  case  of  this  disease  in  which  salicylate  of  soda  is  em- 


188  DISEASES  OF  THE   HEART 

ployed,  and  acute  endocarditis  or  pericarditis  does  not  develop, 
can  any  one  assert  it  would  have  occurred  had  the  remedy  not  been 
administered  ?  Are  there  any  statistics  to  show  that  endocarditis 
has  been  less  frequent  than  before  the  use  of  the  salicylates  ? 
Even  if  one  or  more  series  of  rheumatic  cases  treated  with  this 
remedy  show  a  smaller  percentage  of  endocarditis  than  others  not 
so  treated,  how  can  one  be  sure  that  the  difference  in  results  is  not 
purely  accidental,  since  all  rheumatic  attacks  do  not  inevitably 
lead  to  cardiac  inflammation  ? 

By  all  means  during  a  rheumatic  attack  resort  to  salicylic 
acid,  or  one  of  its  salts,  to  potash  or  soda,  local  applications  to  the 
affected  joints,  to  regulation  of  the  diet,  and  any  other  approved 
means  of  antirheumatic  treatment.  But  do  not  be  too  confident 
that  endocarditis  will  not  develop.  Should  it  not,  consider  your- 
self and  the  patient  fortunate. 

I  confess  to  the  same  scepticism  concerning  the  efficacy  of 
local  treatment  of  the  prtccordium,  as  leeches,  blisters,  and  cold  ap- 
plications, in  preventing  acute  endocardial  inflammation.  The 
only  prophylactic  measure  that  appeals  to  me  as  rational  is  the  pro- 
curement of  as  much  rest  to  the  heart  as  possible,  by  keeping  the 
patient  quiet  during  his  attack  of  rheumatism,  that  the  valves  may 
not  suffer  trauma  by  reason  of  strain.  Fortunately,  in  an  acute 
attack  of  severity  the  urgency  of  the  symptoms  compels  the  patient 
to  remain  at  rest ;  but  in  eases  of  subacute  rheumatism,  particu- 
larly if  an  old  valvular  defect  already  exists,  the  patient  should 
be  urged  to  remain  at  rest,  so  as  to  lessen  the  tension  of  the  valves 
and  the  possibility  of  having  inflammation  rekindled  in  them. 
This  is  often  irksome  to  the  patient,  but  if  he  has  the  reason  ex- 
plained to  him  he  is  likely  to  acquiesce,  although  perhaps  with  no 
very  good  grace.  Even  after  all  the  rheumatic  syni})toms  have 
disappeared  the  patient  should  be  cautioned  against  violent  exer- 
cise, and  should  be  kept  under  rather  frequent  observation,  that 
the  earliest  evidence  of  endocarditis,  sliouM  such  arise,  may  not 
be  overlooked. 

Upon  the  occurrence  of  acute  endocarditis,  or  of  subjective  or 
objective  symjjtoms  sus])i('ious  of  such  an  inflammation,  tlie  pa- 
tient should  prom])tly  l)e  juit  to  bed,  if  not  there  already,  and  kept 
there  as  quiet  as  possible,  both  mentally  and  physically.  The  ob- 
ject of  this  is  apparent ;  bodily  exertion  as  well  as  mental  excite- 


ACUTE   ENDOCARDITIS  189 

ment  augments  the  frequency  of  cardiac  contractions  and  subjects 
the  valve-curtains  to  increased  strain.  The  same  principles  should 
apply  to  the  treatment  of  inflamed  valves  as  to  that  of  inflamed 
joints.  The  use  of  the  latter  not  only  causes  pain,  but  intensifies 
the  inflammation.  Unfortunately,  the  heart  cannot  be  put  at  en- 
tire rest,  but  by  slowing  its  contractions  its  diastole  or  period  of 
rest  is  lengthened  and  its  contractions  are  less  violent.  Theoret- 
ically, at  least,  the  inflammatory  process  would  thus  be  less  active 
and  the  danger  lessened  of  rupture  of  the  inflamed  and  tender 
cusps,  or  of  dislodgment  of  a  soft,  not  firmly  seated  thrombus,  and 
the  formation  of  embolism.  If  the  heart's  action  is  violent  or  too 
rapid,  attempt  should  be  made  to  quiet  it  by  placing  ice-bag  to 
the  prseeordium  or  by  the  administration  of  bromides. 

Digitalis  is  very  commonly  administered  for  this  purpose,  but 
it  cannot  be  stated  too  emphatically  that  this  drug  is  inadmissible 
in  the  treatment  of  acute  endocarditis.  It  not  only  does  no  good, 
but  is  positively  harmful.  Although  capable  of  slowing  the  heart, 
digitalis  at  the  same  time  increases  the  strength  of  systole,  and 
thereby  subjects  the  valves  to  more  than  ordinary  strain.  The 
benefit  to  be  derived  from  a  slowing  of  the  contractions  is  offset 
by  the  injury  to  the  valves  and  by  other  dangers  possible  from 
this  more  forcible  closure,  as  already  explained.  It  is  better  to 
let  the  heart  keep  its  own  gait  than  attempt  to  control  it  by  possi- 
bly injurious  means. 

Aconite  or  veratrum  viride  are  likewise  injurious,  but  in  a 
different  way.  They  are  depressors  to  the  myocardium ;  and  if  this 
be  inflamed  or  weakened  by  serous  infiltration,  there  is  danger  of 
these  drugs  causing  serious  dilatation.  The  same  objection  can- 
not be  urged  against  the  local  employment  of  cold,  and  as  a  matter 
of  fact  this  therapeutic  agent  is  highly  praised  by  those  who  have 
given  it  an  extended  trial.  As  stated  in  the  chapter  on  Acute 
Pericarditis,  the  ice-bag  is  preferable  to  cloths  wrung  out  in  ice- 
water,  since  they  do  not  subject  the  patient  to  the  danger  of  taking 
cold  by  wetting  the  clothing,  and  for  the  same  reason  are  more 
comfortable.  The  ice-bag  should  not  be  applied  directly  to  the 
bare  skin,  but  a  dry,  light  cloth  should  be  interposed.  Should  the 
heart  and  circulation  have  become  very  feeble,  cold  had  better 
not  be  resorted  to,  because  cardiac  depressors  are  no  longer  indi- 
cated. 


190  DISEASES   OP   THE   HEART 

Hot  applications  to  the  piwcordiiim  are  then  more  serviceable 
on  account  of  the  stimulating  effect  they  produce.  Vesication  of 
the  prsecordium,  either  in  the  form  of  one  large  blister,  or  of  re- 
peated small  blisters,  is  a  treatment  that  once  met  with  much 
favour,  but  is  objectionable,  since  it  occasions  more  nervous  irri- 
tation than  it  is  likely  to  do  good.  The  application  of  mustard 
or  the  tincture  of  iodine  or  of  a  turpentine  stupe  are  less  objec- 
tionable because  less  severe,  and  are  sometimes  capable  of  alleviat- 
ing pain. 

Mercurials  and  tartar  emetics  are  now  known  to  exercise  no 
restraining  influence  over  the  inflammatory  process,  and  are  there- 
fore no  longer  used  by  the  best  authorities.  Moderate  doses  of 
iodide  of  potash  have  been  recommended,  in  the  hope  of  restricting 
the  formation  or  promoting  the  absorption  of  the  inflammatory 
products.  It  is,  however,  doubtful  if  this  remedy  possesses  any 
such  influence  in  the  course  of  acute  endocarditis. 

When  medicines  are  powerless  to  cut  short  an  attack,  or  even 
probably  to  diminish  its  severity,  we  are  left  to  a  purely  symp- 
tomatic treatment.  Pain  and  restlessness  should  be  alleviated  by 
the  use  of  opium,  and  in  the  case  of  adults  morphine  hypoder- 
mically  is  the  best  mode  of  administration.  In  children  great 
care  must  be  exercised  in  its  use,  and  it  is  always  well  to  first  try 
the  efficacy  of  bromides  in  conjunction  with  cold  applications  and 
soothing  liniments.  Antipyrine,  phenacetiiie,  and  other  remedies 
of  this  class  are  capable  of  exerting  depression,  and  if  employed 
at  all  should  be  in  small  doses  and  with  strychnine  or  some  stimu- 
lant. 

The  pyrexia  of  acute  simple  endocarditis  is  usually  not  high, 
and  therefore  such  anti})yretics  are  not  likely  to  be  needed  for 
the  reduction  of  temperature.  If  this  should  become  necessary,  it 
would  be  best  attempted  by  judicious  sponging.  Insomnia  may 
be  prevented  by  bromide,  paraldehyde,  sulphonal,  or  trional,  or, 
best  of  all,  by  some  preparation  of  opium. 

So  soon  as  the  endocardium  is  found  to  be  the  seat  of  acute 
inflammation  the  physician  should  constantly  bear  in  mind  the 
possibility  of  the  heart  finally  succumbing  tlirough  weakness,  if 
not  structural  change  of  the  myocardium.  The  organ  should  be 
sustained,  therefore,  by  that  best  of  all  heart-tonics,  strychnine. 
Opium  is  also  a  heart-tonic,  and  wliilo  being  given  for  the  relief 


ACUTE  ENDOCARDITIS  191 

of  j^ain,  also  supports  the  heart,  provided  it  be  not  administered 
with  greater  frequency  or  in  larger  doses  than  are  required  to 
alleviate  the  symptoms.  Sulphate  of  strychnine  is,  hov^ever,  the 
remedy  on  which  chief  reliance  should  be  placed.  Given  in  mod- 
erate doses,  at  first  -gV  of  a  grain  to  an  adult  three  times  a  day,  it 
may  be  increased  to  -sq,  or  even  to  -^-q,  if  signs  of  myocardial 
weakness  supervene.  Should  the  disease  assume  a  grave  charac- 
ter, and  attacks  of  threatening  asystolism  make  their  appearance, 
by  cyanosis,  feeble  and  irregular  pulse,  paroxysms  of  dyspnoea,  or 
signs  of  pulmonary  oedema,  the  heart  should  be  promptly  stimu- 
lated by  ammonia,  camphor,  ether,  brandy,  and  the  like.  Inhala- 
tions of  oxygen  may  also  be  resorted  to,  and  are  likely  to  prove 
temporarily,  if  not  permanently,  beneficial. 

The  patient's  general  strength  should  likewise  be  sustained  by 
nutritious,  though  light,  diet.  Milk,  beef  juice,  an  occasional  raAv 
egg,  soup,  broth,  and  wine  jelly  are  all  serviceable.  A  cup  of 
soup  (prepared  from  Mosquera's  beef  jelly),  tropon  and  somatose, 
form  admirable  adjuvants  to  the  dietary.  The  nourishment 
should  be  given  frequently,  every  two  to  three  hours,  and  in  small 
amounts,  care  being  taken  to  avoid  all  articles  of  diet  which  occa- 
sion gaseous  distention  of  the  stomach  and  intestines.  Constipa- 
tion should  not  be  permitted,  and  even  if  the  action  of  the  bowels 
is  regular,  benefit  is  likely  to  accrue  from  the  occasional  adminis- 
tration of  a  blue  pill  or  small  dose  of  calomel,  followed  by  a  gentle 
saline  aperient.  The  urine  should  be  watched,  and  if  it  become 
bloody  or  albuminous  the  diet  should  be  restricted  to  milk,  and 
the  patient  urged  to  drink  freely  of  pure  water. 

Acute  Ulcerative  Endocarditis. — Fortunately  there  are  grada- 
tions in  the  severity  of  this  type  of  the  affection;  were  it  not  so 
the  physician  would  be  but  a  helpless  spectator  of  the  ravages  of 
this  dreadful  malady.  Indeed,  such  is  his  attitude  in  severe  cases, 
or  in  those  that  have  made  considerable  progress  before  recog- 
nition of  their  true  nature.  The  first  duty  of  the  medical  attend- 
ant is  to  search  for  the  cause — that  is,  the  source  of  the  primary  in- 
fection— and,  if  this  is  discovered  and  can  be  removed  by  surgical 
interference,  to  promptly  resort  to  such  treatment.  This,  alas! 
is  not  generally  possible ;  but  if,  as  Sir  Douglas  Powell  thinks,  un- 
sanitary environment  and  exposure  to  sewer-gas  emanations  are 
■capable  of  setting  up  fresh  infection  in  a  case  of  old-standing  valvu- 


192  DISEASES   OF   THE   HEART 

lar  disease,  tlien  the  patient  should  be  promptly  removed  to  a 
healthful  location. 

The  next  indication  is  to  resort  to  ever}-  means  which  affords 
any  hope  of  re-enforcing  tissue  resistance,  as  a  nutritious  and 
easily  assimilated  diet.  The  lines  of  treatment  already  laid  down 
for  the  sustaining  of  the  heart  and  protecting  it  against  the  injury 
resulting  from  unnecessary  work  in  the  simple  form  are  equally 
applicable  to  the  ulcerative.  Indeed,  they  are  still  more  urgently 
required;  for  not  only  is  inflammation  more  destructive  and  likely 
to  invade  the  myocardium,  but  even  when  this  escapes  ulceration 
or  abscess  formation  the  heart-muscle  is  likely  to  suffer  from  the 
enfeebling  effect  of  the  toxaemia. 

In  severe  cases  the  prostration  of  the  patient  generally  calls 
for  the  administration  of  small,  frequently  repeated  doses  of 
brandy  or  ammonia.  The  use  of  alcohol  in  conditions  of  sepsis  is 
very  generally  ennDloyed,  and,  in  the  opinion  of  many  clinicians, 
is  highly  useful.  Some  indeed  advocate  whisky  in  large  and  fre- 
quently administered  amounts.  Strychnine  should  be  given  in  full 
doses,  and  will  yield  the  best  results  if  administered  hypodermic- 
ally.  Quinine  was  formerly  exhibited  in  doses  of  15,  20,  or  more 
grains  for  the  control  of  the  fever;  but  with  a  clearer  knowledge 
of  the  etiology  and  pathology  of  this  affection,  we  now  know  that 
this  remedy  can  exert  no  controlling  influence  over  its  course. 
Iron  and  arsenic  have  also  been  employed,  and  Powell  speaks 
highly  of  the  latter,  not  as  a  curative  agent,  but  simply  as  a  car- 
diac and  general  tonic. 

Attempts  have  been  nuide  to  introduce  into  the  system  antisep- 
tics in  sufficient  quantity  to  exert  at  least  a  modifying  influence 
upon  the  sepsis.  The  one  deserving  special  mention  is  sulpho- 
carbolate  of  soda,  which  has  been  thought  in  mild  cases  to  exert 
a  favourable  influence.  Sansom  has  reported  one  case  in  which 
dui'iug  its  use  such  iiii])rovcment  took  ]dace  that  the  patient  left 
the  hospital ;  she  returned,  however,  and  succumbed  to  a  fresh 
attack  or  accession  at  the  end  of  ten  months,  "  At  the  autopsy 
the  diagnosis  of  septic  endocarditis  was  confirmed,  the  mitral, 
tricuspid,  and  aortic  valves  being  diseased  and  infiltrated  with 
micrococci." 

Drechfeld,  in  speaking  of  this  remedy  in  4-drachm  doses,  men- 
tions a  case  reported  by  Sansom  (probably  the  one  just  quoted) 


ACUTE  ENDOCARDITIS  193 

in  which,  when  death  took  place  at  a  later  period,  "  distinct  cica- 
tricial tissue  was  found  at  the  site  of  the  old  ulcerations." 

If  this  or  any  other  antiseptic  remedy,  as  salol  and  salophen,  is 
to  do  good,  it  must  be  in  very  large,  frequently  repeated  doses,  so 
as  to  rapidly  bring  the  system  under  their  influence,  and  should 
then  be  continued  for  a  considerable  time.  These  latter  remedies 
recommend  themselves  in  cases  with  a  rheumatic  element,  because 
composed  of  salicylic  as  well  as  carbolic  acid;  but  the  depressing 
effect  of  the  former  upon  the  myocardium  must  not  be  forgotten. 
For  my  part  I  am  inclined  to  attribute  whatever  benefit  has 
seemed  to  follow  such  treatment  to  their  local  antiseptic  action 
upon  the  intestinal  tract.  Fermentative  processes  and  diarrhoea, 
as  shown  by  foetor  of  the  discharges,  are  very  common  within  the 
digestive  tube  of  patients  suffering  from  sepsis.  Such  a  condition 
may  not  only  intensify  the  pyrexia  and  other  symptoms  of  infec- 
tion, by  itself  setting  up  an  infection  of  intestinal  origin,  but  it 
prevents  the  proper  digestion  and  assimilation  of  nourishment. 
If  now  this  putrefactive  fermentation  can  be  prevented  by  intes- 
tinal antisepsis,  the  patient's  nutrition  will  improve  and  his  tissue 
resistance  be  augmented.  It  is  possible,  perhaps,  by  having  this 
additional  enemy  thus  removed,  the  system  may  be  able  to  cope 
successfully  with  the  primary  invader.  At  all  events,  the  physi- 
cian should  employ  these  and  every  other  means  that  afford  possi- 
ble chance  of  improvement  in  dealing  with  so  formidable  an  ad- 
versary. 

The  universal  success  of  the  antitoxin  treatment  of  diphtheria, 
and  the  encouraging  reports  that  have  come  from  the  use  of  anti- 
streptococcus  serum  in  some  cases  of  pyaemia  and  puerperal  sej)- 
ticsemia,  indicate  the  dawn  of  a  new  era  in  theraj)eutics.  It  is  to 
be  hoped  that  in  the  not  very  distant  future  we  shall  possess  a 
serum  potent  against  each  kind  of  pus-producing  microbe.  At 
present  we  are  limited  to  the  serum  just  mentioned;  and  inasmuch 
as  the  streptococcus  is  the  agent  frequently  at  work  in  cases  of 
septicaemia,  and  the  judicious  employment  of  this  serum  appears 
not  to  be  injurious,  we  are  certainl}^  warranted  in  giving  it  a  trial 
in  cases  of  septic  endocarditis.  This  has  already  been  done, 
although  to  what  extent  I  am  not  able  to  say,  nor  have  I  been 
able  to  find  how  many  cases  of  this  disease  treated  in  this  manner 
have  appeared  in  the  literature  to  date. 


194  DISEASES  OF   THE   HEART 

Douglas  Powell  has  tabulated  14  cases  of  ulcerative  endocar- 
ditis in  which  antistreptococcns  serum  has  been  employed  in  Lon- 
don. The  results  are  as  follows:  Three  recoveries,  9  deaths,  and 
2  in  which  no  favourable  result  ensued.  Powell  is  of  the  opinion 
that  these  results  appear  more  discouraging-  than  they  really  are, 
from  the  fact  that  the  serum  was  employed  in  the  late  stages  of 
the  disease,  owing  to  a  natural  hesitancy  to  try  a  new  remedy, 
and  after  "  large  embolic  detachments  had  set  up  fresh  centres  of 
cultivation  in  many  positions,"  He  concludes  therefore:  "  It  may 
be  laid  down  as  a  principle,  governing  treatment  by  this  particular 
serum,  that  the  more  distinct  the  history  of  a  previous  endocardial 
lesion  and  a  subsequent  exposure  to  an  infection  through  a  suppu- 
rative medium,  or  a  sewer-gas  sepsis,  the  more  appropriate  the 
case  for  the  treatment.  This  rule  would  discourage  its  employ- 
ment in  cases  in  which  the  pneumococcus,  gonococcus,  or  some 
other  microbes  divergent  in  character  from  the  streptococci  and 
staphylococci  were  concerned ;  and  if  with  the  recognition  of  this 
principle,  and  its  earlier  and  bolder  carrying  out,  more  encourag- 
ing results  are  obtained,  it  will  certainly  follow  that  analogous 
measures  will  be  found  for  the  circumvention  of  the  other  forms 
of  microbic  action." 

If  the  primary  source  of  infection,  an  abscess  for  instance,  be 
not  discovered,  and  therefore  not  removed  by  the  surgeon,  or  if 
fresh  emboli  laden  with  pus  cocci  repeatedly  discharge  into  vari- 
ous parts  of  the  system,  to  maintain  the  already  existing  sepsis  or 
set  up  fresh  centres  of  infection,  then  assuredly  antistreptococcns 
serum  will  prove  of  little  or  no  beneiit. 

If,  on  the  contrary,  the  patient  is  suffering  from  pyaemia,  the 
original  portal  of  infection  having  been  closed,  and  no  fresh  intoxi- 
cation having  taken  place,  then  this  serum  would  be  of  service, 
even  though  the  streptococcus  be  not  the  only  microbe  concerned 
in  the  process.  With  this  formidable  streptococcus  disposed  of, 
the  system  ought,  theoretically  at  least,  to  be  able  to  cope  success- 
fully with  the  other  kind  of  bacteria.  Of  course,  hope  of  recov- 
ery or  even  improvement  can  only  be  entertained  in  comparatively 
mild  cases,  or  when,  as  Powell  says,  the  disease  is  recognised  and 
treatment  begun  early.  A  process  with  a  pronounced  destructive 
tendency  cannot  probably  be  checked,  but  there  are  cases  of  septic 
endocarditis  which  are  shown  by  the  clinical  history  to  be  not  thus 


ACUTE   ENDOCARDITIS  195 

rapidly  destructive  or  malignant.  Since  no  one  can  foresee  how 
virulent  the  endocarditis  is  to  prove,  the  patient  should  be  given 
the  benefit  of  a  doubt,  and  the  serum  tried.  Gibson  suggests  that 
in  every  case  an  examination  of  the  blood  should  be  made  for 
possible  detection  by  culture,  inoculation,  experiment,  or  other- 
wise of  the  nature  of  the  infective  agent;  but  their  detection,  it 
must  be  remembered,  is  extremely  unlikely. 

Endocardial  inflammation  following  pneumonia,  or  in  which 
the  pneumococcus  has  been  identified,  promises  no  hope  of  im- 
provement from  this  treatment.  It  is  to  be  hoped  that  we  shall 
possess  some  day  an  eflicient  antipneumococcus  serum,  and  indeed 
the  researches  of  the  Klemperer  brothers  and  others  afford  some 
promise  of  this  being  attained. 

Personally  I  have  had  but  little  experience  with  antistrepto- 
coccus  serum  in  acute  endocarditis.  The  wife  of  a  physician  had 
suffered  for  years  from  an  aortic  regurgitation  of  rheumatic  origin. 
At  the  time  I  saw  her  she  had  been  ill  for  several  weeks  with 
moderate  fever  of  a  remittent  type  that  fluctuated  between  about 
100°  and  102°  F.,  or  a  little  more.  She  complained  much  of 
prtecordial  distress  and  paroxysms  of  pain,  also  of  pain  in  the  lower 
extremities  about  the  joints,  although  the  latter  were  not  appre- 
ciably swollen  or  tender.  The  usual  antirheumatic  remedies — sal- 
icylates, alkalies,  etc. — did  not  appear  to  exert  any  influence  over 
the  affection,  and  as  I  believed  she  was  suffering  from  fresh  endo- 
carditis, possibly  of  a  septic  type,  I  advised  a  trial  of  antistrepto- 
coccus  serum.  This  was  obtained  from  St.  Louis,  and  was  given 
in  two  doses  of  10  cubic  centimetres  each.  Her  husband  subse- 
quently sent  me  a  report,  from  which  the  following  has  been 
extracted: 

"  Mrs.  B.  had  been  very  sick  about  one  month  when  you  saw 
her.  The  attack  set  in  with  a  spell  of  tachycardia,  lasting  be- 
tween three  and  four  days,  pulse-rate  near  200  during  all  that 
period.  The  joints  were  only  slightly  inflamed,  temperature  about 
102°  F.,  with  but  slight  variation.  I  gave  two  doses  of  antistrepto- 
coccus  serum  three  days  apart,  as  you  directed,  without  immediate 
effect  on  temperature  or  symptoms.  At  end  of  two  weeks,  how- 
ever, temperature  subsided  nearly  to  normal.  A  very  heavy  ery- 
thematous rash  followed  the  use  of  the  serum.  She  gradually 
crept  from  her  perilous  condition,  dropsy  disappeared,  appetite 


196  DISEASES  OF  THE   HEART 

returned  with  a  fair  degree  of  strength.  She  had  a  good  deal  of 
bronchitis,  and  was  much  worse  after  you  saw  her  than  she  was 
then.  No  one  who  saw  her  at  her  worst  thought  she  could  possibly 
recover." 

The  nature  of  this  ease  was  very  doubtful,  and  from  Dr.  B.'s 
report  the  serum  appears  to  have  been  of  doubtful  utility.  Yet 
I  recall  distinctly  having  subsequently  met  another  practitioner,, 
who  had  been  present  at  the  time  of  my  examination,  and  who 
stated  in  no  unequivocal  terms  that  in  his  opinion  the  serum  had 
been  of  benefit. 

About  a  year  ago  I  saw  in  consultation  with  Dr.  Lovewell  a 
man  of  about  forty  who  had  been  ill  for  a  number  of  weeks  with 
an  intermittent  fever,  rigors,  and  sweatings,  symptoms  of  cardiac 
disease,  and  distinct  evidence  of  an  aortic  valve-affection,  which 
had  not  existed  before  his  illness.  The  origin  of  the  infection 
could  not  be  ascertained.  There  were  well-marked  signs  of  aortic 
insufficiency,  which  from  the  general  septic  phenomena  and  albu- 
minuria could  not  have  been  other  than  a  malignant  endocarditis. 
As  everything  in  the  line  of  antiseptics  had  been  tried  to  no  pur- 
pose, I  advised  the  use  of  anti streptococcus  seriim.  The  patient 
survived  a  number  of  weeks  longer,  but  died  suddenly  as  a  result 
apparently  of  emotional  excitement.  I  did  not  see  the  patient 
again,  but  had  news  of  his  condition  from  Dr.  Lovewell,  who 
stated  more  than  once  that  under  the  use  of  the  serum  the  tem- 
perature became  lower,  less  irregular,  and  the  other  indications 
of  sepsis  less  pronounced.  In  fact,  the  general  condition  im- 
proved so  much  that  tlie  doctor  at  one  time  began  to  entertain 
the  hope  of  his  patient's  ultiniato  recovery. 

It  will  be  remembered  that  in  the  case  reported  of  my  patient 
of  forty,  who  died  of  pulmonary  infarcts,  this  serum  was  likewise 
employed.  It  failed  to  exert  any  other  effect  than  to  slightly  re- 
duce temperature  and  produce  a  feeling  of  somewhat  greater 
strength.  In  this  instance  it  was  not  used  until  late  in  tlie  illness 
and  after  embolic  phenomena  had  more  than  once  aj^jpeared,  I 
regret  that  the  treatment  with  the  serum  was  not  begun  earlier^ 
although  I  am  very  doubtful  if  it  would  have  materially  affected 
the  ultimate  result.  These  experiences  are  too  limited  to  be  of 
value  in  forming  an  estimate  of  the  utility  of  the  serum,  but 
inasmucli    as    its    use    was    not    attended    by    unpleasant    effects 


ACUTE   ENDOCARDITIS  197 

I  shall  certainly  continue  to  give  it  a  trial  whenever  this  seems 
indicated. 

Such  cases  are  so  desperate,  and  the  prospect  of  recovery  so 
slight,  that  I  believe  one  is  justified  in  resorting  to  whatever 
affords  even  a  chance  of  benefit ;  and  if  an  old  preparation  is  em- 
ployed, there  is  not  much  danger  of  producing  erythema  or  articu- 
lar inflammation,  and  the  remedy  cannot  prove  more  harmful 
than  the  disease  itself,  unchecked. 

J.  Michell  Clarke  has  reported  a  case  of  a  woman  of  twenty- 
two  who  had  had  an  attack  of  rheumatism  at  eighteen,  followed 
by  left-sided  pleurisy  with  effusion.  She  complained  of  weakness, 
dyspncjea,  pra^cordial  pain,  and  oedema  of  the  ankles.  While  under 
treatment  for  these  symptoms  she  had  a  sudden  chill,  followed  by 
a  temperature  of  103°  F.  After  remaining  high  for  four  days 
the  temperature  fell  to  normal,  and  after  so  remaining  for  about 
a  week,  again  rose,  and  prevailed  for  nine  days  with  a  very  irregu- 
lar course.  There  was  a  systolic  apex-murmur,  another  loud  sys- 
tolic murmur  in  the  pulmonary  area,  and  a  faint  diastolic  one  at 
the  right  base.  Bacteriologic  examination  of  the  blood  from  a  vein 
was  negative.  A  diagnosis  of  ulcerative  endocarditis  was  made, 
and  treatment  with  antistreptococcus  serum  was  instituted.  In- 
jections were  given  from  December  31,  1899,  to  February  9,  1900, 
sometimes  daily,  at  other  times  every  other  day,  and  once  five 
days  intervened  between  injections.  The  doses  varied  from  10 
cubic  centimetres  to  20  cubic  centimetres,  though  as  a  rule  15 
cubic  centimetres  were  given.  The  patient  recovered,  and  exami- 
nation revealed  the  apex  in  the  fifth  interspace  nipple-line  with  a 
loud,  blowing  murmur  throughout  the  prtecordium  and  posterior- 
ly, but  loudest  in  the  aortic  area. 

Douglas  Powell  speaks  of  the  administration  of  yeast,  and  re- 
ports a  case  in  which  recovery  appeared  to  be  due  to  this  remedy. 
It  is  probable  that  the  efficacy  of  yeast  is  due  to  the  nuclein  of 
the  yeast-cell,  therefore  in  Vaughan's  yeast-nuclein  we  possess  a 
preparation  more  efficient  than  a  solution  of  yeast.  This  may  be 
administered  either  by  the  mouth  or  rectum,  a  solution,  ISTo.  2, 
being  specially  prepared  for  this  purpose,  or  solution  No.  1  may 
be  injected  under  the  skin  up  to  60  or  80  minims  in  the  course  of 
the  day.  ISTuclein  or  nucleinic  acid  acts  by  increasing  the  number 
of  the  polynuclear  leucocytes,   which   are  the   forms  chiefly  in- 


198  DISEASES  OF  THE  HEART 

creased  in  the  leiicocytosis  observed  in  infection,  and  by  the  in- 
crease  of  which  the  germicidal  action  of  the  blood  is  avigmented. 

Many  encouraging  reports  have  been  made  of  the  favourable 
effects  of  yeast-nuclein  in  cases  of  pus-infection  and  cryptogenetic 
infection.  I  employed  it  in  one  case  of  acute  endocarditis  super- 
vening upon  an  old  valvular  lesion,  which  followed  a  follicular  ton- 
sillitis, that  may  have  been  rheumatic,  but  if  so  was  the  only  mani- 
festation of  rheumatism.  The  remedy  was  administered  by  the 
rectum,  owing  to  the  patient's  dread  of  hypodermic  injections. 
Under  its  influence,  or  at  least  during  its  administration,  the  mild 
pyrexia  which  liad  existed  for  about  ten  days,  without  showing 
indication  of  subsiding,  gradually  sank  to  normal.  The  patient 
subsequently  died.  From  the  foregoing  it  is  evident  that  the 
most  the  physician  can  do  in  the  treatment  of  acute  endocarditis 
is  to  aid  nature  by  helping  to  maintain  the  vital  powers  and  by 
removing  obstacles  that  lie  in  nature's  way. 


CHAPTER    V 
CHRONIC    ENDOCARDITIS 

Morbid  Anatomy. — Two  forms  of  chronic  endocarditis  are 
fonnd,  one  the  result  of  the  proliferative  processes  following  an 
acute  inflammation,  and  the  other  a  part  of  a  general  fibroid  trans- 
formation of  the  vascular  system,  arteriosclerosis. 

In  the  form  following  the  acute  disease  the  development  of 
fibrous  tissue  begins  with  the  organization  of  the  vegetations  and 
thrombi  that  have  formed  in  the  earlier  stages.  As  a  rule  the 
vegetations  are  for  the  most  part  absorbed,  but  the  process  of  or- 
ganization leaves  a  slight  nodular  thickening  on  the  surface  of 
the  endocardium.  The  formation  of  new  connective  tissue  goes 
much  further  than  the  mere  repair  of  the  acute  lesions,  however, 
for  what  reason  we  cannot  say,  and  the  entire  substance  of  the 
valve  is  infiltrated  by  fibrous  tissue,  which  in  the  course  of  time 
undergoes  contraction  that  causes  a  thickening  and  deformity 
of  the  valve-cusps.  This  process,  then,  though  initially  of  an  in- 
flammatory nature,  eventuates  in  a  sclerosis. 

The  second  form  is  of  sclerotic  origin  from  the  beginning,  and 
is  usually  associated  with  a  similar  process  in  the  blood-vessels, 
particularly  the  arteries.  In  this  process  the  aortic  valve  is  the 
one  most  frequently  involved,  and  the  process  seems  to  be  often 
a  direct  extension  of  the  disease  from  the  aorta.  It  is,  however, 
by  no  means  rare  to  find  the  mitral  valve  involved,  and  often  both 
are  affected  together. 

The  stiffening  and  deformity  of  the  valve-leaflets  leads  to  dis- 
turbance of  their  function  in  two  ways :  The  segments  may  be 
retracted  or  their  edges  curled  in  such  a  way  as  to  permit  the  pas- 
sage of  blood  in  the  wrong  direction  (Regurgitation).  The  con- 
dition is  then  spoken  of  as  insufiiciency,  incompetence,  or  regurgi- 
tation.   If,  however,  the  deformity  of  the  valve  is  of  such  a  nature 

199 


200  DISEASES   OF  THE   HEART 

as  to  cause  a  narrowing  of  the  orifice,  the  condition  is  known  as 
stenosis.    . 

Stenosis  may  be  brought  about  by  thickening  and  rigidity  of 
the  valve-segments  so  that  they  cannot  open  perfectly  for  the 
passage  of  the  blood,  or  the  remains  of  vegetations  or  thrombi, 
which  have  undergone  organization  or  calcification,  may  encroach 
on  the  opening.  The  special  ways  in  which  these  lesions  are  pro- 
duced will  be  considered  in  detail  under  the  head  of  the  individual 
valvular  diseases.  It  should  be  noted  here,  however,  that  stenosis 
of  an  ostium  and  incompetency  of  the  corresponding  valve  are 
usually  associated  conditions,  though  as  a  rule  one  or  the  other 
predominates  and  gives  its  character  to  the  lesion. 

Fibroid  thickening  of  the  mural  endocardium  is  not  uncom- 
mon in  connection  with  chronic  valvulitis,  especially  of  the  sclero- 
tic type.  It  may  also  occur  as  a  part  of  an  interstitial  myocar- 
ditis. The  membrane  is  thickened  and  of  an  opaque  whitish  or 
yellowish  colour — the  latter  when  fatty  change  is  prominent. 
Mural  endocarditis  is  often  associated  with  dilatation  of  a  heart- 
cavity,  and  is  then  probably  due  to  the  stretcliing  of  the  membrane. 

The  secondary  changes  in  chronic  valvulitis  are  mainly  those 
due  to  the  circulatory  disturbance  occasioned  by  the  stenosis  or  in- 
competence, as  the  case  may  be.  If  a  valve  is  incompetent  it  per- 
mits regurgitation  into  the  chamber  behind  during  its  diastole, 
and  this  cluunbor  then  receives  blood  from  two  sources,  the  normal 
one,  and  tlirough  the  iiieouijx'tent  valve.  Sucli  an  oversupply  of 
blood  leads  to  an  overdistention  of  the  chamber,  and  to  an  in- 
creased efi"ort  in  order  to  completely  empty  itself.  The  continu- 
ance of  these  conditions  leads  to  a  permanent  increase  in  the  capa- 
city of  the  chamber,  while  the  increased  work  thrown  on  the 
musculature  of  the  wall  causes  an  increase  in  its  strength  and 
1 1 1  ick ness  ( Hypertrophy ) . 

If  the  deforming  process  results  in  stenosis,  the  chamber  heliind 
the  defect  e.x])criences  increased  ditHculty  in  expelling  its  contents, 
and  develops  hypertrophy  of  the  kind  known  as  concentric,  because 
associated  with  little  or  no  dilatation.  The  chamber  in  front  of  a 
stenosed  orifice,  on  the  otiier  hand,  is  ajit  to  become  atro]>hied  and 
reduced  in  size,  since  it  receives  a  diminished  supply  of  blood,  and 
its  work  is  corres|)oii(liiigly  lessened. 

The  (listiii'l):ni('('s  of  circulation  secondary  to  valvular  disease 


CHRONIC  ENDOCARDITIS  201 

are  by  no  means  limited  to  the  heart  itself,  but  affect  the  various 
oi'gans  and  tissues  of  the  body.  The  blood-supply  to  the  arteries 
is  lessened,  obstruction  to  discharge  of  blood  from  the  veins  exists, 
and  thus  is  induced  passive  congestion,  which  affects  not  only  the 
organs  drained  by  the  veins,  but  in  vi^ell-marked  cases  also  the 
arterial  system  which  supplies  them.  In  the  course  of  time  this 
congestion  reacts  injuriously  on  the  heart  in  a  manner  to  be  fur- 
ther elaborated  under  the  head  of  the  respective  valve-lesions. 

Acute  endocarditis  is  often  found  associated  with  the  chronic, 
and  indeed  the  latter  predisposes  markedly  to  the  former.  Changes 
in  the  myocardium  are  also  frequent,  usually  in  consequence  of 
nutritional  disturbance,  which  is  secondary  to  the  dilatation  and 
hypertrophy,  or  to  associated  atheroma  of  the  coronary  arteries. 
Pericarditis  is  also  not  infrequently  associated  with  chronic  endo- 
carditis, and  is  generally  of  the  adhesive  variety.  This  is,  of 
course,  due  to  the  two  diseases  having  had  the  same  remote 
origin. 

Etiology. — The  strictly  sclerotic  form  of  endocarditis  is  not 
of  microbic  origin,  but  is  either  an  expression  of  nutritional 
change  incident  to  age,  gout,  renal  and  vascular  disease,  or  is  the 
result  of  strain.  That  some  individuals  evince  a  family  tendency 
to  sclerotic  changes  in  the  entire  circulatory  apparatus,  as  well  as 
in  the  kidneys,  appears  proved  by  the  frequent  observation  of 
atheromatous  valvular  disease  in  two  or  more  members  of  the  same 
family. 

Age  is  thought  to  be  a  factor  in  the  causation  of  this  form  of 
chronic  valvular  disease;  and  yet  the  occurrence  of  the  disease  in 
some  individuals  at  a  comparatively  early  age  indicates  that. there 
is  some  other  influence  at  work  besides  senility. 

Chronic  endocarditis  is  so  frequently  observed  in  persons  of  a 
distinctly  arthritic  habit  that  gout  has  come  to  be  regarded  as  an 
important  etiological  element.  With  respect  to  such  gouty  influ- 
ence, it  seems  to  me  that  it  is  rather  the  entire  manner  of  living 
which  has  to  be  taken  into  account.  For  example,  I  recently  ex- 
amined a  physician's  father,  whose  case  illustrates  what  I  mean 
very  well. 

Dr.  W.,  from  the  interior  of  Illinois,  brought  his  father  to 
me  with  the  following  history :  The  patient  Avas  a  German,  sixty- 
nine  years  of  age,  who  had  enjoyed  robust  health  up  to  two  years 
15 


202  DISEASES   OF   THE   HEART 

before,  at  which  time  he  developed  redness  and  swelling,  with 
some  pain  of  the  great-toe  joints.  This  was  regarded  as  gouty, 
and  nnder  appropriate  therapeutic  and  dietetic  management  dis- 
appeared. Six  months  before  his  visit  to  me  he  began  to  complain 
of  shortness  of  breath  upon  exertion,  whereupon  his  son  made  an 
examination  of  the  lieart  and  detected  a  murmur.  The  routine 
treatment  w^ith  digitalis,  strychnine,  nitroglycerine,  and  cathartics 
had  failed  to  produce  appreciable  benefit,  and  twice  there  had  been 
expectoration  of  bloody  sputum.  During  the  previous  two  weeks 
he  liad  had  two  nocturnal  attacks  of  dyspnoea  that  came  on  in  the 
small  hours,  while  still  a  third  took  place  after  an  evening  meal. 
The  son  furthermore  stated  what  was  of  special  interest  from  an 
etiological  standpoint — viz.,  that  his  father  had  always  led  a  seden- 
tary life,  getting  exercise  by  driving  instead  of  walking,  had 
always  eaten  heartily  of  rich  food,  indulged  freely  in  beer  and 
other  alcoholic  beverages,  after  the  German  custom,  and  had  been 
a  heavy  smoker,  lie  had  never  had  inflammatory  rheumatism  or 
any  other  illness. 

The  patient  was  a  man  of  i)Owerful  physique,  and  in  spite  of 
his  gray  hair  did  not  look  at  all  like  an  old  man.  Plis  normal 
weight  was  207,  but  at  date  of  examination  was  190  pounds, 
while  his  height  was  G  feet.  His  chest  was  broad  and  deep^  his 
bones  large  and  strong,  the  muscular  system  well  developed,  abdo- 
men not  corpulent,  and  subcutaneous  fat  not  excessive.  The  nails 
were  moderately  ridged,  the  radial  arteries  stiff  but  not  beady, 
the  temporal  and  carotid  arteries  not  stiffened,  and  the  subclavians 
did  not  stand  out  prominently  nor  throb  strongly,  as  they  often 
do  in  old  men.  There  was  a  ])rononnced,  visible,  and  palpable 
epigastric  pulsation  reaching  at  least  2  inches  below  the  xyphoid^ 
cartilage,  but  the  apex-beat  could  not  be  made  out.  In  the  aortic 
area  was  a  systolic  thrill,  palpable  upon  moderate  pressure  during 
expiration.  The  thoracic  parietes  were  so  hard  and  resisting  that 
])ercussion  was  difficult,  but  the  lungs  were  everywhere  resonant 
and  respiratory  sounds  were  faint  and  vesicular.  Absolute  car- 
diac dulness  was  not  increased,  but  by  resort  to  palpatory,  aus- 
cultatory, and  ordinary  plessimetric  percussion,  relative  dulness 
was  found  greatly  increased  upward,  to  the  left,  and  downward, 
but  not  notably  to  the  right.  The  left  border  reached  an  inch 
outside  of  the  left  nipple,  in  all  5  inches  from  the  left  edge  of 


CHRONIC  ENDOCARDITIS 


203 


the  sternum  (Fig.  33).  With  exception  of  the  pubnonic  second 
sound,  itself  feeble,  the  heart-tones  could  not  be  heard.  There 
was,  however,  a  loud  systolic  murmur  of  distinct  sawing  quality 
audible  throughout  the  pra?cordia  and  for  a  distance  beyond  the 
left  nipple  into  the  axillar}^  region.  Upon  careful  study  of  this 
murmur  it  was  found  to  have  two  areas  of  maximum  intensity,  one 
in  the  second  right  interspace  near  the  sternum,  the  other  in  the 
vicinity  of  the  left  nipple.  Moreover,  in  these  two  areas  the  pitch 
Avas  slightly  yet  distinctly  different,  being  lower  and  harsher  in 
the  aortic  and  more  musical  in 
the  mitral  area.  The  heart's 
rate  was  90,  and  its  rhythm 
regular.  The  liver  was  pal- 
pable. 

The  audible  pulmonarv 
second  tone  and  hj^pertrophic 
dilatation  of  the  right  ventri- 
cle confirmed  the  evidence 
obtained  from  the  mitral  mur- 
mur and  established  the  ex- 
istence of  mitral  regurgita- 
tion. The  aortic  systolic  bruit 
and  loss  of  the  aortic  second 
sound,  together  with  the  sys- 
tolic thrill,  gave  evidence  of 
stiffness,    and    perhaps    steno- 


FiG.  33. — Kelative  Uulness,  Case  of 
Cheonic  Endocaeditis  (p.  201). 


sis  of  the  aortic  valves.  The  absence  of  a  rheumatic  history,  the 
patient's  age,  the  late  development  of  symptoms,  the  moderate 
arteriosclerosis,  and  lastly,  the  heart  findings,  all  seemed  to  war- 
rant the  opinion  that  the  valvular  changes  were  due  to  sclerotic 
endocarditis.  The  condition  of  the  kidneys  was  not  ascertained 
at  that  time,  as  the  son  had  not  examined  the  urine,  but  inasmuch 
as  there  was  nocturnal  micturition,  renal  cirrhosis  was  thought 
probable,  and  it  was  advised  to  have  the  urine  collected  for  twenty- 
four  hours  and  examined. 

In  this  case  I  believe  the  cause  lay  in  the  strain  to  which  the 
valves  of  the  left  heart  had  been  subjected  for  man}-  years  in  con- 
sequence of  the  abnormal  blood-pressure  brought  about  by  his  ex- 
cessive consumption  of  food  and  alcoholic  liquids  without  suffi- 


204  DISEASES  OF  THE   HEART 

cient  physical  exercise.    How  much,  if  any,  influence  can  be  attrib- 
uted to  tobacco  and  waste  products  I  cannot  say. 

The  influence  of  strain  has  long  been  recognised  in  the  produc- 
tion of  the  sclerotic  changes  now  being  considered.  High  blood- 
pressure,  lasting  for  years,  is  a  cause  of  yalvular  as  well  as  of 
yascular  strain,  but  inasmuch  as  the  indiyiduals  in  whom  such  in- 
jurious blood-pressure  is  obseryed  generally  lead  inactive  lives, 
dine  well,  and  often  suffer  from  indigestion  and  constipation,  it  is 
likely  that  the  products  of  defective  metabolism  circulating  in  the 
blood  act  as  chemical  irritants,  and  play  a  not  unimportant  part  in 
the  development  of  sclerotic  changes. 

Disease  of  the  aortic  valves  is  frequently  observed  in  men 
who  pursue  laborious  occupations,  as  smiths,  carpenters,  etc.,  and 
hence  arduous  physical  exertion  is  also  accredited  with  the  pro- 
duction of  valvular  and  vascular  strain  and  consequent  sclerosis. 
It  is  in  this  class  of  workers  that  rupture  of  an  aortic  cusp  is  most 
frequently  observed,  with  its  disastrous  sequels.  It  has  always 
seemed  to  me  not  an  easy  thing  to  correctly  estimate  the  influence 
of  physical  strain  in  working  people,  since  they  are  so  often  given 
to  the  immoderate  use  of  alcohol  and  tobacco,  and  frequently  be- 
come victims  of  syphilis.  We  should  probably  consider  that  in 
these  people  all  these  factors  are  at  work,  and  attribute  their 
chronic  endocarditis  to  their  mode  of  life  in  general,  without  at- 
tempting to  isolate  any  one  etiological  factor.  Syphilis  is  un- 
doubtedly capable  of  setting  up  sclerotic  deformity  of  the  valves, 
although  endocardial  changes  follow  luetic  disease  far  less  often 
than  do  myocardial  and  vascular  degeneration. 

Of  that  form  of  chronic  endocarditis  which  is  met  with  in  the 
young,  and  which  is  of  true  inflammatory  origin,  the  one  gl'eat 
cause  is  rheinnatism.  Although  these  valvular  lesions  may  un- 
doubtedly begin  in  an  acute  vegetative  endocarditis,  which  merges 
gradually  into  a  chronic  process,  it  is  often  a  low  grade  of  sub- 
acute inflammation  from  the  beginning  that  brings  about  this 
form  of  chronic  endocarditis.  This  inflammation  may  originate 
in  an  acute  rheumatic  attack,  and  be  recognised  clinically  at  the 
time,  or  it  may  develop  so  slowly  and  insidiously  as  to  create  no 
Bvmptoms,  and  remain  undetected  for  years.  Indeed,  it  is  not  at 
all  uncommon  for  valvular  diseases  originating  in  this  manner  to 
be  first  diagnosed  after  compensation  has  begun  to  wane.     This 


CHRONIC  ENDOCARDITIS  205 

slowly  forming  endocarditis  gives  rise  chiefly  to  stenosis,  and,  in 
accordance  with  the  law  of  numerical  frequency,  to  stenosis  of  the 
left  auriculo-ventricular  orihce. 

Physicians  sometimes  fall  into  the  loose  manner  of  speech  of 
the  laity  and  call  the  pains  of  myalgia  and  an  intractable  or  oft- 
recurring  neuralgia,  rheumatic.  They  should  remember,  however, 
that  these  so-called  rheumatic  pains  are  etiologically  and  patho- 
logically very  different  from  the  articular  rheumatism  that  sets 
up  endocarditis.  When  a  student  in  Munich,  I  questioned  Prof. 
Joseph  Batier  on  this  subject,  and  received  the  emphatic  reply 
that  "  muscular  rheumatism  never  produces  valvular  disease." 
For  further  discussion  of  the  etiology  of  endocarditis  the  reader 
is  referred  to  the  chapter  upon  Acute  Endocarditis  and  those  deal- 
ing with  the  individual  valve-lesions. 

Symptoms. — The  reader  of  the  following  chapters  will 
doubtless  be  impressed  by  the  fact  that  the  different  forms  of 
valvular  disease  present  considerable  similarity  as  regards  those 
derangements  of  circulation  of  a  mechanical  nature  and  those  dis- 
turbances of  visceral  function  which  give  rise  to  subjective  symp- 
toms. Such  differences  as  exist  are  not  so  much  differences  in 
kind  as  in  degree.  Any  one  of  the  valvular  defects  may,  so  long 
as  it  is  perfectly  compensated,  exist  for  years  without  revealing  its 
existence  to  the  consciousness  of  the  patient,  but  when  compensa- 
tory hypertrophy  is  no  longer  adequate,  conditions  result  whicli 
must  of  a  necessity  force  themselves  upon  the  notice  of  the  patient 
with  greater  or  less  prominence. 

In  mitral  disease  the  sensations  are  mainly  due  to  passive 
congestion,  while  in  lesions  at  the  aortic  orifice  they  are  the  result 
of  a  diminished  or  defectively  sustained  supply  of  arterial  blood; 
yet  in  both  it  would  be  inaccurate  to  draw  such  a  strict  divi- 
sion. In  mitral  disease  there  is  defective  arterial  circulation  as 
well  as  venous  stasis,  and  when  in  aortic  valve  defects  compensa- 
tion fails,  there  is  more  or  less  passive  engorgement  added  to  the 
imperfect  arterial  flow.  Consequently,  the  clinical  picture  takes 
its  colouring  from  both  conditions,  but  in  varying  proportions, 
and  hence  in  all  forms  of  valvular  disease  there  comes  a  time  in 
the  stage  of  destroyed  compensation  Avhen  whatever  individual 
features  each  affection  may  have  once  possessed  become  blende'd 
into  the   symptom-complex  of  cardiac   inadequacy  in   its   broad 


206  DISEASES   OF   THE   HEART 

sense.  Some  of  these  eharaeteristies  are  plainly  recognised  as  the 
effects  of  mechanical  pressure  in  the  venous  system,  as  the  dull, 
tense  pain  of  hepatic  congestion,  the  scanty  albuminous  urine,  the 
hsemorrhoidal  congestion  and  fluxes,  and,  in  large  part  at  least,  the 
serous  transudations  and  the  digestive  disorders. 

Other  symptoms  are  probably  owing  to  the  incomplete  elimi- 
nation of  the  normal  products  of  metabolism;  or  to  the  nmnufac- 
ture  and  accumulation  in  the  system  of  abnormal  products  which 
result  from  perverted  function  on  the  part  of  the  stomach,  liver, 
and  other  chylopoietic  viscera;  or  there  is  a  combination  of  these 
various  toxins,  with  a  lessened  supi)ly  of  oxygen  and  other  neces- 
sary nutritive  principles,  that  may  explain  some  of  the  subjective 
phenomena,  such  as  the  dull,  oppressive  headache,  the  insomnia, 
nervousness,  and  in  some  instances  the  low,  muttering,  or  even  ac- 
tive delirium  occasionally  observed  in  the  terminal  stage. 

The  dyspnoea  of  advanced  heart-disease  is  probably  a  manifes- 
tation of  both  mechanical  pressure  in  the  pulmonary  vessels  and 
upon  the  lungs  by  the  dilated  heart  and  by  hydrothorax,  but  also  of 
deficient  oxygenation  through  sluggish  blood-flow  and  from  bron- 
chial obstruction  by  mucus  and  serum.  Since,  then,  so  many 
factors  enter  into  the  production  of  the  nmnifold  symptoms  com- 
plained of  or  manifested  by  sufferers  from  valvular  heart-disease, 
it  is  not  possible  to  satisfactorily  account  for  them  all  or  to  explain 
why  some  are  present  in  one  and  absent  in  another  case. 

We  have  also  to  reckon  with  individual  tendencies,  neuroses, 
intercurrent  affections,  complications,  etc.,  all  of  which  serve  to 
modify  the  legitimate  clinical  picture.  For  example,  I  recall  a 
certain  young  woman  who  first  came  under  my  care  for  an  un- 
compensated mitral  regurgitation  of  rhenmatic  origin  in  1803, 
and  who  during  the  ensuing  five  years  presented  some  highly  in- 
teresting and  puzzling  phenomena. 

At  the  beginning  hers  was  an  urdinarv  case  of  mitral  insuffi- 
ciency with  slight  a?dema.  which  readily  yielded  to  treatment,  and 
she  was  lost  sight  of  for  two  years.  She  then  rea]>iieared,  having 
shortly  before  had  a  recurrence  of  rheumatism,  and  had  thereafter 
Iteen  married,  both  of  which  occurrences  were  unfortunate  for  her. 
( 'om])ensation  was  .so  defective,  probably  in  consequence  of  a  fresh 
endocarditis  whicli  had  passed  beyond  its  acute  stage,  and  which 
coidd  be  recognised  as  having  existed  oidy  by  its  effects,  or  in 


CHRONIC  ENDOCARDITIS  207 

consequence  of  a  pericarditis  that  had  led  to  adhesion  between  the 
sac  and  anterior  chest-wall,  that  the  patient  manifested  both  ascites 
and  anasarca. 

Besides  this  very  obvious  disturbance  of  circulation  she  suf- 
fered greatly  from  insomnia  and  a  degree  of  emotional  instability 
that  could  reasonably  be  considered  hysterical  and  made  her  ex- 
tremely hard  to  control.  But  the  particular  feature  that  puzzled 
me  for  a  time  was  the  fact  that  the  secretion  of  urine,  scanty  at 
all  times,  became  almost  suppressed  whenever  for  the  sake  of 
sparing  the  overburdened  heart  she  was  subjected  to  rest  in  bed. 
Whether  or  not  this  was  due  to  the  abolition  of  those  accessory 
aids  to  venous  How  residing  in  muscular  movements  of  the  lower 
extremities  and  in  deepened  inspiration  incident  to  gentle  exercise 
about  her  apartment  I  could  not  decide,  but  this  seemed  probable 
from  the  subsequent  fact  that  the  enormous  hepatic  engorgement 
and  ascites  did  not  disappear  until  she  was  given  a  course  of  re- 
sistance exercises. 

Pari  passu  with  this  removal  of  the  mechanical  hindrance  to 
circulation  the  insomnia  vanished  and  her  normal  mental  state  re- 
turned. Compensation  was  at  length  regained  and  retained  for  a 
number  of  months.  Six  months  later,  however,  she  suddenly  de- 
veloped an  excruciating  and  obstinate  neuralgia  in  the  course  of 
the  right  brachial  plexus,  for  which  I  could  discover  no  adequate 
cause,  and  which  resisted  all  treatment.  It  was  accompanied  by 
cough  with  scanty  mucous  expectoration,  of  which  repeated  care- 
ful examinations  of  the  heart  and  lungs  failed  to  detect  any  cause 
aside  from  the  old-standing  valvular  lesion.  At  length,  discour- 
aged by  her  failure  to  obtain  relief,  she  returned  to  her  home  in 
the  country,  where  during  the  next  few  weeks  she  expectorated 
masses  of  tenacious  sputum,  which  were  said  when  put  in  water 
to  spread  out  and  look  like  the  branches  of  a  tree.  Whether  this 
was  an  instance  of  fibrinous  bronchitis  or  not  I  cannot  say,  but 
certain  it  is,  that  when  finally  her  bronchitis  subsided  her  neural- 
gia also  disappeared.  I  have  always  believed  this  was  a  manifes- 
tation of  infection,  since,  as  we  know,  cardiac  patients  are  particu- 
larly prone  to  obscure  infections,  and  that  the  neuralgia  could  not 
be  regarded  as  anywise  a  symptom  directly  attributable  to  her 
heart-disease. 

The  next  event  in  this  patient's  series  of  experiences  occurred 


208  DISEASES  OF  THE  HEART 

about  a  year  later.  She  had  again  been  suffering  from  rheuma- 
tism, as  I  was  told,  when,  according  to  her  sister's  statement,  she 
suffered  one  night  from  severe  pain  in  the  region  of  the  heart, 
for  which  hot  cloths  were  being  applied.  Suddenly  the  sufferer 
exclaimed,  "  There !  something  has  broken,  and  the  pain  has  all 
gone."  She  then  seemed  to  sink  away,  her  pulse  becoming  too 
weak  and  rapid  to  be  counted,  her  extremities  cold,  and  her  coun- 
tenance blue.  Stimulants  revived  her,  but  all  night  she  continued 
to  have  sinking  spells,  which  necessitated  the  administration  of 
restoratives. 

The  explanation  of  this  attack  has  never  been  clear  to  me. 
Whether  a  tendinous  cord  snapped,  or  a  pericardial  adhesion  gave 
way,  or  whether  the  pain  may  not  have  been  due  to  a  muscular 
cramp,  I  cannot  say.  Under  the  influence  of  heat  the  muscle  may 
have  suddenly  relaxed,  and  thus  caused  a  sensation,  which  to  the 
suffering  and  highly  nervous  apprehensive  girl  was  naturally  at- 
tributed to  the  heart,  and  threw  her  into  a  condition  of  mental 
shock  which  reacted  on  the  weakened  heart.  At  all  events,  the 
attack  was  fraught  with  no  less  alarm  to  the  friends  than  to  the 
patient,  and  an  explanation  was  sought,  which  could  not  be  given. 

Six  weeks  subsequently  the  patient  was  again  brought  to  the 
city  in  a  truly  deplorable  condition.  There  were  marked  evi- 
dences of  cardiac  asthenia  and  consequent  circulatory  embarrass- 
ment, pronounced  icterus,  oedema  of  the  ankles,  ascites,  enormous 
hepatic  congestion,  o'denia  of  the  left  but  not  the  right  arm,  and 
in  the  heart  signs  of  double  mitral  disease,  relative  tricuspid  in- 
sufficiency, and  adherent  pericardium. 

The  feature  of  chief  interest,  however,  was  connected  with 
the  dropsy  of  the  left  upper  extremity.  This  was  strictly  local- 
ized, extending  from  the  fingers  up  to  and  ceasing  with  the  shoul- 
der. Palpation  of  the  axilla  disclosed  that  the  axillary  vein  had 
been  converted  by  thrombosis  into  a  firm  cord.  To  what  distance 
the  thrombosis  extended  down  the  arm  could  not  be  determined, 
but  it  did  not  involve  the  jugular  veins.  The  "  swelling,"  it  was 
stated,  had  made  its  appearance  a  week  earlier,  but  aside  from  the 
annoyance  did  not  api)oar  to  occasion  pain  or  distress. 

This  highly  interesting  and  coin])ai-atively  rare  condition  was 
an  instance  of  venous  thrombosis  occurring  in  some  cases  of  valvu- 
lar disease.     It  has  formed  the  subject  of  an  instructive  paper 


CHRONIC  ENDOCARDITIS  209 

by  Dr.  William  Welch,  which  was  read  at  the  session  of  the  Asso- 
ciation of  American  Physicians  in  1900.  Welch  was  able  to  col- 
lect but  28  recorded  instances,  including  his  own,  although,  as 
stated  by  him,  the  condition  probably  occurs  more  often  than  it 
is  recognised.  Of  these  28  cases,  all  but  4  involved  the  veins  of 
the  upper  extremities  and  neck,  a  fact  which  lends  to  it  addi- 
tional interest  and  importance.  Twent^'-two  cases  showed  throm- 
bosis of  the  left  side  alone  15  times,  bilaterally  8  times,  while 
only  twice  was  it  confined  to  the  right.  Welch  found  that  the 
thrombosis  might  be  limited  to  the  veins  of  the  arm,  to  those  of 
the  neck,  or  might  involve  all  the  veins — that  is,  the  superior  vena 
cava,  the  innominate,  both  internal  and  external  jugular,  sub- 
clavian, axillary  and  brachial,  and  even,  as  in  one  case,  the  supe- 
rior thyroid. 

Although  thrombosis  uiay  and  does  sometimes  occur  in  indi- 
viduals suffering  from  chronic  arteriosclerosis  and  nephritis,  yet 
in  Welch's  28  cases  there  was  in  every  instance  valvular  disease 
as  follows :  Mitral  regurgitation  9  times,  mitral  stenosis  alone  6 
times,  mitral  stenosis  with  insufficiency  6  times,  and  aortic  regur- 
gitation with  relative  mitral  incompetence  once.  In  10  instances 
there  was  associated  aortic  and  mitral  disease.  The  thrombus 
was  either  red  or  reddish-gray,  and  although  in  some  instances 
it  was  softened  at  its  centre,  it  for  the  most  part  was  firm  through- 
out, and  occluded  the  vessel  excepting  at  its  extremities.  In  one 
case  it  was  a  "  wall  thrombus."  It  is  also  interesting  to  note  that 
the  thrombosis  appeared  to  have  begun  at  the  lower  end  of  the  in- 
ternal jugular  in  those  instances  in  which  it  involved  the  cervical 
veins.  This  fact  led  Welch  to  conclude  that  the  formation  of  the 
thrombus  was  favoured  by  the  peculiar  anatomical  arrangement 
of  the  cervical  veins  on  the  left  side,  together  with  the  conditions 
governing  the  blood-flow  in  them. 

As  pointed  out  by  Ilanot,  the  left  innominate  vein  is  longer 
and  more  oblique  than  the  right,  which,  together  with  the  right- 
angle  junction  of  the  left  internal  jugular  with  the  subclavian 
and  the  bulbous  expansion  of  the  internal  jugular,  favours,  in 
Welch's  opinion,  the  formation  of  eddies  or  whirling  currents  at 
that  point,  and  thus  furthers  the  development  of  thrombosis. 
Moreover,  he  thinks  there  is  probable  pressure  upon  the  sub- 
clavian vein  by  the  dilated  left  auricle  and  dilated  pulmonary 


210  DISEASES  OF  THE  HEART 

veins,  so  that  circulation  in  the  cervical  and  arm  veins  becomes 
extremely  sluggish,  and  thus  provides  another  favouring  factor. 
Finally,  in  one  of  his  cases  Welch  was  able  by  cultures  to  identify 
the  streptococcus  pyogenes,  which,  he  thinks,  warrants  the  hypoth- 
esis that  in  these  cases  there  is  an  infectious  origin  for  the  throm- 
bosis, a  conclusion  which  is  strengthened  by  recent  observations 
going  to  show  that  in  all  cases  of  venous  thrombosis  there  is  an 
infection. 

In  my  case  there  is  good  reason  to  believe  that  the  patient  was 
still  suffering  from  some  infection,  for  she  had  but  a  few  weeks 
earlier  gone  through  with  what  was  called  rheumatism  by  her 
home  physician,  yet  which  may  very  well  have  been  a  strepto- 
coccus infection,  which  so  often  presents  the  appearances  of  artic- 
ular rheumatism.  Moreover,  there  were  three  small,  distinctly  in- 
durated lymphatic  glands  situated  just  above  the  left  clavicle,  near 
the  outer  border  of  the  left  sterno-cleido-mastoid  muscle,  while  the 
patient  displayed  a  slight  elevation  of  temperature.  In  other  re- 
spects my  case  conformed  with  the  most  of  Welch's  requirements 
— namely,  she  was  a  female,  of  but  twenty-three  years  of  age,  and 
was  a  sufferer  from  mitral  disease.  Her  symptoms  too  were  char- 
acteristic in  the  localization  of  the  oedema  to  the  affected  arm 
below  the  location  of  the  thrombosis.  She  did  not,  however,  suffer 
pain,  at  least  not  at  the  time  the  interesting  condition  was  de- 
tected, the  occluded  vein  was  not  tender,  and  I  failed  to  discover 
any  enlargement  and  tenderness  of  the  lymphatics  of  the  arm,  as  is 
often  present.  If  such  existed,  they  were  hidden  from  observa- 
tion by  the  oedematous  condition  of  the  extremity.  Welch  states, 
finally,  that  in  at  least  one  of  the  cases  collected  by  him  there  was 
mild  delirium,  which  was  attributed  to  the  cerebral  oedema  discov- 
ered at  the  autopsy. 

In  the  matter  of  the  diagnosis  of  this  form  of  venous  tlirom- 
bosis  there  is  no  difficulty,  ])rovided  the  thrombosed  vein  can  be 
felt,  and  even  wlien  not,  strictly  localized  dropsy  in  one  arm  or  one 
side  of  the  neck  renders  the  existence  of  thrombosis  very  likely. 
Nevertheless,  according  to  ITanot,  the  greater  length  and  obliquity 
of  the  left  innominate  vein  may  sometimes  cause  unilateral  and 
circumscribed  a'dema  even  when  venous  thrombosis  is  not  present. 

The  prognosis  is  unfavoural^le  to  recovery  from  the  dropsy  if 
the  veins  are  extensively  plugged.     If  the  thrombosis  is  not  com- 


CHRONIC  ENDOCARDITIS  211 

plete,  or  is  of  limited  extent,  it  is  possible  for  collateral  circulation 
to  become  established  and  absorption  to  take  place.  Finally,  the 
condition  is  likely  to  occur  in  the  terminal  stage  of  the  valvular 
disease,  and  if  very  extensive  it  may  contribute  to  the  patient's 
death. 

It  is  not  common  for  patients  witn  chronic  valvular  disease  to 
suffer  from  embolism,  and  yet  such  a  possibility  should  always  be 
borne  in  mind.  It  is  stated  that  such  an  occurrence  is  more  fre- 
quent in  mitral  than  aortic  disease;  and  I  have  under  observa- 
tion a  female  patient  with  mitral  insufficiency  who  has  perma- 
nent contracture  of  the  fingers  of  the  left  hand  and  but  partial 
use  of  the  arm  as  a  result  of  an  embolus  that  was  thrown  off  pre- 
sumably from  her  mitral  valve  nearly  six  years  ago.  The  symp- 
toms of  embolism  are  usually  said  to  be  pain  in  the  part  where 
the  plug  lodges,  nausea,  and  even  vomiting,  a  chill,  and  rise  of 
temperature.  To  judge  from  cases  of  embolism  observed  in  acute 
endocarditis  and  from  pulmonary  infarcts,  I  should  say  that  pain 
in  the  affected  part  is  the  most  constant  symptom. 

The  splenic  artery  is  a  frequent  seat  of  embolism,  and  it  may 
well  be  that  the  transient  pain  from  which  cardiac  patients  not 
infrequently  complain  in  the  region  of  the  spleen  may  be  of  this 
origin.  It  is  unsafe  to  make  such  a  diagnosis,  however,  unless  one 
can  detect  enlargement  and  tenderness  of  this  organ  following  the 
pain.  This  is  emphasized  by  the  fact  that  these  patients  are  very 
prone  to  sudden  and  sharp  pains  of  a  neuralgic  character  in  various 
situations,  particularly  in  the  abdomen. 

I  recall  an  instance  that  was  narrated  to  me  by  an  ophthal- 
mologist of  sudden  blindness  of  one  eye  resulting  from  the  plug- 
ging of  the  retinal  artery,  and  as  the  lady  possessed  a  blowing  sys- 
tolic apex-murmur,  the  embolus  was  thought  to  have  been  a  minute 
vegetation  from  her  mitral  valves.  I  have  also  been  informed  of  a 
young  lady  with  valvular  disease  who,  upon  awakening  one  morn- 
ing, was  found  to  have  lost  during  the  night  all  recollection  of 
certain  members  of  her  own  family.  This  peculiar  lapse  of  mem- 
ory was  attributed  by  her  medical  attendant  to  embolism. 

Pulmonary  infarcts  are  not  at  all  uncommon  in  cases  of  ad- 
vanced valvular  disease,  and  are  evinced  by  sudden  acute  pain  in 
the  affected  lung,  together  with  frequent  cough  and  the  spitting 
of  clear  blood.    These  cases  must  not  be  confounded  with  instances 


212  DISEASES   OP   THE   HEART 

of  ha?moptYsis  due  to  sudden  increase  of  pnlnionarv  congestion,  as 
not  seldom  occurs  in  mitral  patients  who  have  overtaxed  their 
hearts.  In  these  cases  the  history  of  some  exertion  and  the  ab- 
sence of  sudden,  sharp  jiain  will  usually  aid  in  the  differential 
diagnosis.  Embolism  of  tlie  middle  cerebral  artery  is  attended  by 
such  manifest  symptoms  that  there  is  usually  but  little  difficulty 
in  determining  the  cause  of  the  phenomena. 

In  a  single  instance  I  have  observed  the  conjunction  of  true 
epilepsy  with  valvular  disease.  The  patient  was  a  man  of  about 
forty  who  presented  well-marked  signs  of  mitral  stenosis.  His 
valvular  lesion  was  of  rheumatic  origin,  and  his  convulsions  ante- 
dated his  cardiac  disease  by  some  years.  There  was  every  reason 
to  conclude  that  the  association  of  these  two  affections  was  purely 
accidental  as  regards  their  etiology.  The  fits  were  usually  excited 
by  indiscretions  in  diet,  and  required  bromides  for  their  control. 
Although  never  assuming  any  causative  relation  between  the  two, 
I  yet  believed  they  exerted  a  deleterious  influence  upon  each  other. 
I  am  very  certain  that  the  epilepsy  affected  his  mitral  disease 
unfavourably  by  serving  to  maintain  and  aggravate  the  dilatation 
of  the  cardiac  chambers.  Such  cases  as  this  are  not  to  be  regarded 
as  instances  of  cardiac  epilepsy,  which  term  has  been  employed  to 
designate  attacks  of  pra'cordial  pain  accompanied  by  loss  of  con- 
sciousness and  succeeded  by  twitchings  of  the  muscles  of  the  face. 

The  association  of  epilepsy  and  heart-disease  in  my  case  serves 
to  emphasize  the  fact  that  valvular  diseases  may  be  complicated 
and  have  their  clinical  picture  modified  by  other  affections.  I 
speak  of  this  because  inexperienced  jjhysicians  are  apt,  when  treat- 
ing patients  with  valvular  disease,  to  attribute  all  symptoms  to 
the  cardiac  complaint. 

Cardio])aths  frequently  become  anaemic  and  neurotic,  hysteri- 
cal or  neurasthenic,  and  then  complain  of  all  sorts  of  sensations, 
which  it  is  clearly  impossible  to  attribute  to  their  valvular 
affection. 

The  French  describe  what  they  term  "  cardiac  cachexia  "  in 
distinction  froin  cardiac  asthenia,  and  wliich  is  analogous  to  the 
cachexias  of  malignant  or  tuberculous  disease.  They  ascribe  it 
to  some  chemical  change  in  the  blood.  It  is  not  at  all  uncommon 
to  see  cardiac  ])atients  who,  while  presenting  no  very  marked  S}Tnp- 
toms  of  cardiac  ina<lcquacy,  yet  display  an  appearance  of  mal- 


CHRONIC  ENDOCARDITIS  213 

nutrition  that  might  not  inaptly  he  termed  a  cachexia.  In  snch 
there  are  often  symptoms  of  weakness,  inability  to  take  and  assim- 
ilate food,  and  various  other  features  that^  even  if  referable  pri- 
marily to  a  valvular  defect,  are  nevertheless  attributable  to  their 
general  state  rather  than  to  their  heart. 

Patients  with  valvular  disease  sometimes  become  victims  of 
attacks  of  palpitation  and  prsecordial  pain  that  place  them  in  the 
category  of  cardiac  neuroses,  although,  strictly  speaking,  this  term 
should  be  applied  to  cases  in  which  the  attacks  are  independent 
of  any  discoverable  heart-disease.  At  such  times  there  may  even 
be  irregularity  or  intermittence  of  the  pulse.  This  is  naturally 
thought  due  to  the  cardiac  lesion,  and  yet  it  may  be  wholly  inde- 
pendent of  the  heart  disorder,  being  the  result  of  some  toxin  per- 
haps, or  of  some  obscure  nervous  excitation.  This  is  proved  by 
the  observation  that,  when  the  attack  subsides,  the  heart's  action 
returns  to  its  former  regular  and  tranquil  state.  I  recall  such  an 
instance  in  a  young  man  with  a  mitral  regurgitation  who  was  sub- 
ject to  attacks  of  palpitation  that  invariably  threw  him  into  a 
perfect  panic  of  fright  and  apprehension.  Yet  when  his  attacks 
subsided  he  resumed  his  ordinary  duties  without  a  symptom  of 
his  cardiac  lesion. 

I  am  in  the  habit  of  assuring  such  patients  that  their  attacks 
of  palpitation  are  not  indicative  necessarily  of  a  serious  state  of 
the  heart — for  persons  without  any  demonstrable  cardiac  disease 
often  manifest  similar  disturbance — but  that  because  the  heart 
is  not  structurally  sound,  it  is  more  easily  thrown  out  of  balance 
by  indigestion  or  other  conditions  that  would  not  be  noticed  were 
it  in  perfect  health.  ]^othing  is  worse  for  cardiopaths  than  to 
get  into  a  state  of  introspection  and  constant  apprehension.  I 
have  known  some  who  were  so  alarmed  over  their  valvular  defect 
that  they  might  be  said  to  be  possessed  by  a  veritable  phobia. 
Such  patients  not  only  imagine  all  sorts  of  symptoms  that  play  no 
part  in  the  clinical  history  of  their  particular  lesion,  but  they  are 
afraid  to  venture  out  alone  lest  they  get  an  attack  or  be  brought 
home  dead.  The  medical  adviser  should  therefore  carefully  dis- 
tinguish symptoms  due  to  the  valve-defects  from  those  that  belong 
to  some  associated  disorder,  and  reassure  the  patient  accordingly. 

Before  completing  this  Subject  I  desire  to  add  a  few  remarks 
concerning  derangements   in   the   rhvthm   of  the  heart's   action. 


214  DISEASES   OF   THE   HEART 

Irregularity  and  intermittenee  of  the  pulse  are  common  in  all 
forms  of  valvular  disease,  yet  they  are  by  no  means  always  ob- 
served. The  regular  and  rhythmic  contraction  of  the  heart-muscle 
depends  upon  its  receiving  regular  and  uniform  stimulation  by 
the  presence  of  the  blood.  Doubtless  there  are  many  disturbing 
factors  of  which  we  are  yet  ignorant,  and  which  may  be  transient 
in  action,  such  as  emotional  or  other  impulses  acting  through  the 
nervous  system,  toxins  of  various  kinds,  etc.  But  aside  from  these 
there  are  degenerative  or  other  alterations  of  the  cardiac  muscle 
itself  that  lead  to  arrhythmia.  Such  a  persistent  derangement  of 
the  pulse  is  therefore  an  unfavourable  omen.  It  is  quite  likely 
to  be  observed  in  mitral  disease,  particularly  regurgitation,  it  is 
said.  Why  this  is,  is  not  clear,  unless  it  is  dependent  upon  dila- 
tation or  degeneration  of  the  auricles. 

A  mere  lack  of  uniformity  in  the  force,  volume,  and  frequency 
of  the  pulse-waves,  to  which  form  of  arrhythmia  is  applied  the 
term  irregularity,  is  far  less  serious  than  intermittenee,  by  which 
is  meant  a  dropping  out  of  some  of  the  pulse-waves.  This  lat- 
ter may  be  due  to  actual  intermissions  in  the  cardiac'  contrac- 
tions, or  it  may  be  caused  by  the  failure  of  all  the  blood-waves  to 
reach  the  wrist,  the  heart  itself  beating  regularly  all  the  time, 
although  with  unequal  force.  Many  interesting  varieties  of  pulse- 
rhythm  have  been  described,  but  I  do  not  know  that  they  possess 
any  special  clinical  significance  aside  from  the  fact  of  their  being 
an  indication  of  disordered  cardiac  action.  Thus  pulsus  alternans 
is  a  term  employed  to  describe  an  irregularity  consisting  in  the 
appearance  first  of  a  large  and  then  of  a  small  wave  that  follow 
each  other  in  regular  succession.  When  the  pulse-waves  occur  in 
pairs  that  are  separated  by  distinct  intervals  they  are  spoken  of 
as  pulsus  higeminus,  and  when  in  groups  of  three  as  pulsus  tri- 
geminus. Pulsus  intercidens  or  intercurrens  denotes  the  occur- 
rence or  interpolation  of  occasional  small  waves  between  the  regu- 
larly occurring  large  waves.  Pulsus  tardus  is  a  slow  pulse,  mag- 
nus  a  large  pulsQ,  parvus  a  small  pulse,  etc. 

These  variations  may  exist  alone  and  for  a  considerable  time, 
or  they  may  be  blended  and  display  tlieir  individual  characters 
for  but  a  few  seconds;  so  that  a  pulse  results  that  is  strikingly 
irregular  and  difficult  or  impossible  to  count. 

It  has  been  my  observation  that  when  a  patient  with  organic 


CHRONIC  ENDOCARDITIS  215 

heart-disease  displays  a  persistently  arrhythmic  pulse  he  is  usu- 
ally not  aware  of  its  existence  by  any  sensations  within  his  chest. 
On  the  contrary,  persons  with  so-called  functional  derangement 
are  very  apt  to  experience  a  sensation  as  if  the  heart  jumped  or 
turned  over  whenever  it  intermits. 

In  studying  the  pulse  in  any  case  of  valvular  disease  it  is  not 
only  necessary  to  observe  its  rhythm,  but  one  should  take  particu- 
lar notice  of  its  force  and  volume.  In  conditions  of  stenosis  the 
pulse  is  very  likely  to  be  small  and  of  poorly  sustained  tension, 
showing  that  the  arterial  system  is  defectively  flushed.  In  some 
cases,  however,  of  mitral  stenosis  the  pulse  is  small  and  tense  in 
consequence  of  obstruction  to  the  flow  of  blood  out  of  the  capil- 
laries. Peculiarities  of  the  pulse  of  aortic  regurgitation  will  be 
dwelt  upon  at  some  length  in  that  section. 


CHAPTER    YI 
MITRAL    REGURGITATION 

By  this  temi  is  designated  an  abnormal  escape  or  leakage  of 
blood  from  the  cavity  of  the  left  ventricle  through  the  left  au- 
riculo-ventricular  orifice  into  the  left  auricle.  Such  regurgitation 
may  be  due  to  structural  defect  of  the  valves  or  to  their  relative 
incompetence  from  dilatation  of  the  ventricle,  or  to  imperfect 
function  on  the  part  of  their  muscular  apparatus.  In  this  chap- 
ter will  be  considered  only  the  form  due  to  valvular  defect. 
Other  terms  applied  to  this  disease  are  mitral  incompetence  or 
insufficiency;  but  inasmuch  as  the  term  regurgitation  is  more 
commonly  employed  in  this  country,  this  is  the  one  that  has  been 
selected  and  is  prefeiTed. 

Morbid  Anatomy. — The  structural  changes  of  the  mitral 
valve  permitting  regurgitation  of  the  blood  are  mainly  thicken- 
ing of  the  cusjjs  with  increased  rigidity  that  prevents  perfect  co- 
aptation, or  the  shortening  or  retraction  of  one  or  both  of  the 
leaflets  in  such  a  way  as  to  permit  the  reflux  of  blood.  The 
segments  lose  their  normal  pinkish  transparent  appearance,  thin 
delicate  feel,  and  become  thickened,  stiff,  and  of  an  opaque  whitish 
or  grayish  colour.  Contraction  of  the  fibrous  tissue  may  cause 
retraction  or  shortening  of  one  or  both  of  the  cusps,  or  curling  of 
their  edges  in  a  manner  to  prevent  etrective  closure  of  the  valve. 
In  the  valvular  disease  following  acute  endocarditis  the  shrivelled 
and  often  calcified  remains  of  old  vegetations  may  be  found  on  the 
auricular  surface  of  the  valve  along  the  line  of  maximum  contact. 
When  these  old  vegetations  are  numerous  the  mitral  ring  is  usu- 
ally fibrous  and  contracted,  leading  to  a  condition  of  stenosis  as 
well  as  regurgitation  (Fig.  34).  Very  commonly,  also,  the  ten- 
dinous cords  are  found  more  or  less  matted  together,  stiffened,  and 
shortened,  so  as  to  still  further  interfere  with  perfect  action  of  the 
valve.  The  deposit  of  calcareous  matter  is  by  no  means  limited  to 
216 


MITRAL  REGURGITATION 


217 


the  old  vegetations,  but  may  affect  the  valve-cusps,  the  chordEe 
tendina?,  or  even  the  mural  endocardium  in  the  neighbourhood. 
In  fact,  the  deposit  of  lime-salts  may  in  some  instances  be  so 


Fig.  34. — Shows  Condition  of  Mitral  Valve,  causing  Kegukgitation  and 
Obstkuction.    Left  Auricle  has  been  dissected  away. 

extensive  as  to  convert  the  entire  valvular  apparatus  into  a  firm 
■calcareous  mass,  having  no  resemblance  whatever  to  the  original 
structure. 

The  local  changes  in  the  endocardium,  however,  form  but  a 
small  part  of  the  morbid  changes  found  in  a  case  of  mitral  insuffi- 
ciency. The  changes  in  the  circulation,  and  the  effect  on  the 
heart-wall  and  on  the  other  organs  of  the  body  that  were  consid- 
ered in  a  general  way  under  chronic  endocarditis,  take  place  here 
and  require  description.  Whenever  mitral  regurgitation  occurs  a 
portion  of  the  contents  of  the  left  ventricle  is  forced  back  during 
systole  into  the  left  auricle,  which  at  the  same  time  is  receiving 
the  normal  flow  of  blood  from  the  pulmonic  veins.  The  chamber 
is  consequently  surcharged,  and  as  the  two  streams  enter  it 
during  its  diastole  it  becomes  overdistended.  At  the  same  time, 
in  consequence   of  its   dilatation,   the   auricle   has  greater  work 

to    perform    in    emptying    itself    of    this    increased    amount    of 
16 


218  DISEASES   OF  THE   HEART 

blood,  and  in  accordance  with  the  physiological  law  that  an 
organ  which  has  increased  work  to  do  will,  so  long  as  its  nutri- 
tion is  unimpaired,  manifest  increased  power  for  work,  the 
walls  of  the  auricle  at  length  become  thicker  and  stronger.  In 
time,  therefore,  the  auricle  comes  to  be  both  hypertrophied  and 
dilated. 

If  these  changes  in  the  circulation  come  on  slowly,  and  time 
is  afforded  for  compensatory  changes  in  the  heart  to  develop,  the 
nutrition  of  the  heart-muscle,  and  indeed  the  integrity  of  the  cir- 
culation, may  suffer  no  serious  injury.  Furthermore,  if  the  auri- 
cle is  able  to  deliver  an  increased  volume  of  blood  to  the  ventricle^ 
this  chamber  is  able  to  discharge  into  the  aorta,  in  spite  of  the 
regurgitation,  an  approximately  normal  amount  of  blood,  and  ade- 
quate arterial  circulation  is  maintained.  So  far,  then,  the  hyper- 
trophy and  dilatation  of  the  auricle  compensates  the  valvular  de- 
fect, which  may  consequently  exist  for  a  long  time  without  pro- 
ducing any  inconvenience. 

If,  however,  the  leakage  is  extreme,  or  if  it  becomes  so  with 
lapse  of  time  and  the  auricle  is  unable  to  completely  empty  itself, 
a  residue  remains,  which  interferes  with  the  inflow  of  blood  from 
the  pulmonary  veins.  Thus  takes  place  an  accumulation  of  blood 
(passive  congestion)  which,  acting  as  increased  peripheral  resist- 
ance to  the  work  of  the  right  ventricle,  leads  to  hypertrophy 
and  dilatation  of  this  chamber.  Moreover,  the  stasis  within  the 
lungs  induces  in  them  the  condition  known  as  brown  induration, 
in  which  the  connective-tissue  elements  are  increased,  the  veins 
engorged,  and  the  whole  organ  is  of  a  dark-brown  colour  in  conse- 
quence of  pigment  deposited  by  the  disintegrating  blood.  In  ad- 
vanced stages  there  may  also  be  pulmonary  o'dema  and  hydro- 
thorax  from  transudation  of  serum  out  of  the  engorged  vessels. 
There  is  always  more  or  less  bronchial  congestion  in  consequence 
of  stasis  within  the  pulmonic  vessels. 

When  at  length  blood-pressure  in  the  pulmonary  artery  grows  ex- 
cessive, the  wall  of  the  right  ventricle  finds  its  work  too  great,  and, 
yielding  to  the  strain,  permits  dilatation  to  supersede  hypertrophy. 
This  chamber  is  now  unal)le  to  fully  empty  its  cont<»nts,  stasis  within 
it  grows,  and  at  length  causes  tricuspid  leakage  either  from  mus- 
cular incompetence  of  the  valve  or,  more  often,  from  great  dilata- 
tion of  the  ventricle.   In  cases  of  long  standing  and  extreme  pressure 


MITRAL   REGURGITATION  219 

in  the  pulmonary  artery,  stretching  of  its  ostium  is  also  occa- 
sioned, and  leads  to  relative  pulmonary  incompetence. 

So  long  as  the  left  auricle  and  right  ventricle  are  capable  of 
coping  successfully  with  the  back  wash  from  the  left  ventricle  the 
work  of  the  right  auricle  is  not  especially  increased.  When,  on 
the  contrary,  the  right  ventricle  begins  to  yield  to  the  strain,  par- 
ticularly when  it  becomes  dilated,  back  pressure  is  exerted  upon 
the  right  auricle  and  great  venous  system.  Veins  everywhere 
grow  more  or  less  turgescent,  and  the  internal  organs  display  the 
effects  of  engorgement.  The  liver  in  particular  becomes  enlarged 
and  in  time  indurated,  and  on  section  shows  the  peculiar  mottling 
that  has  given  to  the  organ  in  this  condition  the  name  of  nutmeg- 
liver. 

In  the  stomach  and  intestines  passive  congestion  leads  to 
chronic  catarrh  of  the  mucosa,  and  in  the  kidneys  to  cyanotic  in- 
duration or  even  chronic  nephritis.  ISTone  of  the  internal  viscera 
escape,  while  the  veins  share  in  the  distending  effects  of  stasis 
and  become  relatively  larger  than  the  arteries.  Back  pressure 
creeps  downward  into  the  vessels  of  the  lower  extremities,  and  as 
circulation  grows  still  more  sluggish  serous  transudation  finally 
makes  its  appearance.  Commencing  in  the  feet,  dropsy  gradually 
extends  upward,  invades  the  peritoneal  cavity  and  walls  of  its 
contained  viscera,  and  in  extreme  cases  the  serous  cavities  within 
the  chest,  and  finally  the  lungs  (Fig.  35).  Thus  far  we  have  con- 
sidered the  secondary  effects  that  are  produced  behind  the  seat  of 
the  original  lesion.  There  are,  in  addition,  certain  effects  of  mitral 
regurgitation  in  front  of  the  lesion.  These  are  the  hypertrophy 
and  dilatation  of  the  left  ventricle  found  in  cases  of  free  and  un- 
combined  mitral  insufficiency.  This  enlargement  seems  rather  re- 
markable at  first  thought,  since  one  would  naturally  think  the 
chamber  ought  to  be  smaller  rather  than  larger  in  size.  At  one 
time  this  condition  of  hypertrophic  dilatation  was  explained  on 
the  hypothesis  that  in  consequence  of  venous  and  capillary  stasis 
blood-pressure  was  increased  in  the  arterial  system,  and  that  hence 
there  was  augmented  intraventricular  pressure  which  resulted  in 
dilatation,  with  increased  demand  for  work  which  led  to  hyper- 
trophy. 

This  theory  is  now  known  to  be  incorrect,  and  has  been  re- 
placed by  the  following:  Owing  to  the  abnormal  volume  of  blood 


2^^  DISEASES  OF   THE   HEART 

•  1  ot  tl^p  clo^e  of  its  diastole,  tliis 
contained  by  the  left  ^-'-'^'^^IJ^'^X  di-harges  with  great 
cha>nber,  which  has  "econ-  hjpemopto  ^^_^^^.^^^      ^^.^ 

force  an  unnatural  amount  of  Wood 


Cyanosis  of  face 


Cyanosis,  and  clubbing 
of  fingers 


Congestion   and   cedema 
of  lungs 


Engorgement   of    portal 
system 


Congestion   and    (i-dema 
of  lower  limbs. 


Fio.  35.— Diagram  si 


V..■,rrT^   ON    THE    ClUCVLATIO 


N    UK    A    MlTllAI.   LkaK. 


MITRAL    REGURGITATION  221 

cavity  is  in  a  state  of  diastole  wlien  it  receives  this  inrush,  and, 
being  relaxed,  becomes  after  a  time  dilated.  At  the  same  time 
it  is  forced  to  handle  a  larger  volume  of  blood,  which  it  can  only- 
do  by  nndergoing  hypertrophy,  and  thns  at  last  this  ventricle 
comes  in  its  turn  to  feel  the  secondary  effects  of  the  circulatory 
disturbance. 

In  time,  moreover,  when  stasis  has  become  everywhere  aj^par- 
ent,  the  left  ventricle  undergoes  still  further  dilatation,  for  which 
it  has  become  prepared  by  certain  structural  changes  within  its 
inyocardiuin.  Its  myocardium  is  flabby  and  of  a  brown  instead 
of  the  normal  beefy  red  colour,  while  its  fibres  are  found  micro- 
scopically to  be  reduced  in  size  and  to  contain  granules  of  brown 
pigment,  especially  near  the  nucleus.  This  increased  dilatation  of 
the  ventricle  at  this  time  is  explained  by  some  as  due  to  the  high 
blood-pressure  in  the  arterial  system  secondary  to  stasis  in  the 
veins,  which  abnormal  arterial  blood-pressure  interferes  with  the 
easy  emptying  of  the  ventricle.  This  is  a  defective  explanation, 
however,  since  physiologically  the  abnormal  blood-pressure  in  the 
venous  system  leads  to  lowered  instead  of  heightened  blood-pres- 
sure in  the  arteries.  The  dilatation  of  the  left  ventricle  is  now 
due  to  the  weakness  of  its  own  wall,  which  does  not  permit  it  to 
completely  empty  its  cavity  with  each  systole.  Thus  is  estab- 
lished a  residue  which  augments  the  amount  of  blood  received 
from  the  auricle  with  the  next  diastole,  while  at  the  same  time  its 
wall  is  powerless  to  withstand  the  dilating  force  of  this  stream 
that  pours  into  it.  Thus  is  at  length  set  up  a  vicious  circle  in 
consequence  of  wdiich  the  effect  of  the  original  valvular  incom- 
petence intensifies  the  regurgitation. 

The  typical  heart,  then,  of  mitral  insufficiency  is  enlarged. 
The  enlargement  is  mostly  of  the  right  ventricle,  and  the  organ 
has  in  consequence  a  rounded  apex.  The  tricuspid  orifice,  and 
often  the  pulmonary,  is  found  to  be  wider  than  usual,  owing  to 
the  dilatation  of  the  right  ventricle.  The  left  ventricle  is  mod- 
erately and  the  left  auricle  greatly  enlarged,  while  the  mitral 
valve  shows  the  structural  changes  already  described,  which  have 
been  the  cause  of  the  whole  trouble. 

Etiology. — What  has  already  been  said  concerning  the  causa- 
tion of  chronic  endocarditis  applies  equally  to  mitral  insufficiency, 
since  this  is  but  one  of  the  manifestations  of  that  affection.    I  shall 


222  DISEASES   OF   THE   HEART 

therefore  only  add  a  few  general  considerations  bearing  on  the 
localization  of  the  deforming  process  at  the  mitral  orifice. 

Incompetence  of  the  left  auriculo-ventricular  valve  is  a  verv 
frequent  cardiac  affection — is  indeed  the  most  frequent  of  all 
vahadar  defects.  This  is  particularly  the  case  in  children  and 
young  adults,  forming  in  this  period  of  life  the  counterpart  in 
point  of  frequency  of  the  sclerotic  changes  at  the  aortic  orifice  in 
persons,  chiefly  men,  past  middle  age.  The  influence  of  childhood 
and  youth  in  the  generation  of  mitral  regurgitation  lies  doubtless, 
not  in  the  fact  of  the  age,  per  se,  but  in  the  prevalence  in  the 
young  of  those  diseases,  inflammatory  rheumatism,  chorea,  and 
the  exanthemata,  which  set  up  endocarditis.  The  greater  liability 
of  the  mitral  than  of  the  aortic  valves  to  suffer  from  endocardial 
inflammation  in  the  earlier  decades  of  life  is  probably  owing  to 
their  being  exposed  to  relatively  greater  strain,  which  their  more 
delicate  structure  fits  them  less  well  to  endure. 

As  regards  sex,  it  is  generally  stated  that  mitral  regurgita- 
tion is  more  fre(pient  among  males  than  females,  but  in  analyzing 
m}''  case-records  I  find  no  predominance  of  either  sex.  After 
throwing  out  all  cases  that  from  the  history,  age,  or  symptoms 
cannot  be  safely  considered  as  organic,  there  remain  126  cases  in 
which  regurgitation  was  due  to  structural  alteration  of  the  valves. 
These  were  divided  equally  between  the  two  sexes.  Classifying 
these  126  cases  according  to  decades,  there  were  6  boys  and  6  girls 
between  one  and  ten  years  of  age,  12  males  and  16  females  be- 
tween ten  and  twenty,  18  of  each  sex  between  twenty  and  thirty, 
14  each  between  thirty  and  forty,  and  15  males  and  7  females 
over  forty.  Examined  with  reference  to  rheumatism  and  other 
diseases,  it  was  found  that  32  males  and  28  females  gave  a  history 
of  rheumatism  alone,  4  males  and  6  females  of  scarlatina  alone, 
5  males  and  4  females  of  measles  alone,  1  female  of  chorea  alone, 
while  of  more  than  one  disease  1  male  and  8  females  had  had 
rhcuiiiatism  and  scarlatina,  4  each  had  had  rheumatism  and  mea- 
sles, and  4  each  rheumatism,  scarlatina,  and  measles,  2  males  and 
5  females  scarlatina  and  measles,  2  females  measles  and  pertussis, 
and  1  f'ciiialc  all  four  diseases,  2  males  and  5  females  chorea,  in 
combination  with  some  of  the  other  diseases  mentioned.  Two 
males  gave  a  history  of  venereal  disease.  Of  the  remaining  cases, 
in  which  no  definite  history  of  previous  disease  could  be  elicited, 


MITRAL   REGURGITATION  223 

the  organic  nature  of  the  lesion  was  rendered  probable  either  bv 
the  existence  of  arteriosclerosis  or  by  the  youthful  age  of  the  pa- 
tient and  the  absence  of  anaemia  or  other  factors  pointing  to  a  rela- 
tive mitral  insufficiency. 

Symptoms. — The  presence  or  absence  of  distinctively  cardiac 
symptoms  dejDends  upon  the  degree  of  the  leak  and  of  the  com- 
pensatory hypertrophy  that  has  been  established.  Consequently 
we  have  to  distinguish  cases  in  which  subjective  manifestations 
of  circulatorv  disturbance  are  wanting  from  those  in  which  there 
is  more  or  less  evidence  of  cardiac  inadequacy.  In  the  former 
class  such  symptoms  as  are  complained  of  are  probably  referable 
indirectly  to  the  valvular  defect,  but  are  nevertheless  such  as  we 
encounter  in  persons  without  disease  of  the  heart.  In  some  in- 
stances they  direct  the  experienced  physician's  attention  to  the 
possibility  of  mitral  disease,  while  in  others  they  seem  to  point 
rather  to  disorders  of  other  organs,  and  the  discovery  of  the  re- 
gurgitation is  accidental.  In  such  cases  the  individual  first  learns 
of  his  malady  on  applying  for  life  insurance,  or  upon  subjecting 
himself  to  physical  examination  prej)aratory  to  athletic  training,  or 
wpon  consulting  his  physican  for  some  trifling  ailment.  The  dam- 
age to  the  valve  is  slight  and  compensatory  hypertrophy  is  perfect. 
It  would  in  some  instances  be  better  for  such  persons  not  to  be 
informed  of  their  defect,  since  although  they  are  able  to  endure 
games  of  skill  and  considerable  exertion,  as  tennis,  without  con- 
scious symptoms,  they  are  likely  after  learning  of  their  lesion,  par- 
ticularly if  of  a  nervous,  excitable  temperament,  to  be  alarmed 
by  palpitation,  which  prior  to  their  knowledge  did  not  attract 
their  attention. 

In  other  instances  regurgitation  is  free,  yet  there  is  a  truly  re- 
markable absence  of  subjective  consciousness  of  its  existence. 
This  is  generally  due  to  the  completeness  of  the  compensatory 
hypertrophy  on  the  part  of  the  right  ventricle  and  the  left  auricle. 
Yet  I  have  known  individuals  of  a  not  very  impressionable  tem- 
perament who,  in  spite  of  rather  inadequate  compensation,  were 
unconscious  of  symptoms  referable  directly  to  their  mitral  dis- 
ease. Some  excitable  neurotic  persons,  like  those  first  alluded  to, 
consult  physicians  for  symptoms  referable  to  the  digestive  tract, 
or  nervous  system,  rather  than  to  the  heart  itself.  These  are 
anorexia,  or  discomfort  after  food,  constipation,  or  an  irregular 


224  DISEASES   OF  THE   HEART 

State  of  the  bowels,  distressing  pra?cordial  pains,  which  either  set 
up  or  are  accompanied  by  palpitation,  and  which  greatly  alarm  the 
patient  and  friends.  In  a  multitude  of  such  cases  there  is  no 
objective  evidence  of  loss  of  compensation,  and  the  patients  are 
able  to  enjoy  outdoor  sports  or  to  participate  in  feats  of  endurance 
without  subjective  symptoms. 

Again,  cases  occur  in  which  the  only  symptoms  are  such  as  are 
usually  classed  under  the  head  of  lithiemia,  or  the  irregular  mani- 
festations of  gout,  and  occurring  in  persons  of  sedentary  habits^ 
are  removed  by  regular  outdoor  exercise. 

In  other  cases  the  most  that  can  be  said  is  they  appear  to  have 
an  unstable  nervous  system,  and  their  symptoms  in  nowise  differ 
from  those  of  other  individuals  of  the  same  category  whose  hearts 
are  healthy.  In  all  such  the  valvular  lesion  does  not  appear  to  be 
directly  responsible  for  the  manifestations,  and  yet  it  may  well 
be  that  these  can  be  referred  to  defective  nutrition  and  elimination 
in  consequence  of  the  circulatory  disturbance. 

It  is  not  uncommon  for  females  with  organic  mitral  insuffi- 
ciency to  present  evidence  of  simple  secondary  anaemia  or  of  chlo- 
rosis without  symptoms  of  cardiac  inadequacy.  If  in  such  cases 
there  is  shortness  of  breath  u])on  unusual  exertif>n,  it  is  no  greater 
than  may  reasonably  be  attributed  to  the  blood-state.  I  recall  a 
remarkably  interesting  and  instructive  instance  of  this  kind.  In 
March,  1901,  a  young  married  lady  of  twenty- four  sought  my 
opinion  because  of  "  a  grating  sound  in  the  heart,"  which  first 
attracted  her  notice  in  the  fifth  month  of  her  pregnancy,  and  which 
still  annoyed  her  at  times  of  unwonted  physical  effort,  as  during- 
rapid  walking.  Aside  from  this  symptom,  there  was  nothing  that 
made  her  conscious  of  her  heart.  She  admitted  getting  a  little  out 
of  breath,  but  this  was  so  slight  she  had  not  given  it  any  attention. 
Both  her  parents  had  died  of  ])ulm(»nary  tuberculosis,  but  of  her 
brothers  and  sisters,  seven  in  all,  none  had  shown  signs  of  the  dis- 
ease. She  had  had  pneumonia  when  but  a  year  old,  scarlatina  at 
eight,  measles  and  ])ertussis  in  childhood,  but  never  rheunmtism, 
and  up  to  the  time  of  her  marriage,  at  twenty-two  years  of  age,  she 
had  considered  herself  well,  Ix'iug  able  to  romp  and  play  like  other 
children  without  trouble.  With  exception  of  the  "  grating  sound  " 
jnentioned,  her  pregnancy  and  confinement  had  been  uneventful, 
and  she  could  not  recall  having  suff'ered  from  more  dyspnoea  than 


MITRAL  REGURGITATION  225 

do  other  women  towards  the  later  months  of  pregnancy.  She  had 
nursed  her  baby  for  nine  months,  and  during  that  period  lost  29 
pounds,  of  which  seven  had  been  regained  in  the  seven  months  fol- 
lowing the  weaning  of  her  infant.  Her  appetite  was  poor,  bowels 
were  irregular,  and  she  was  aj^t  to  suffer  from  sour  stomach  and 
eructations.  The  menses  were  regular  but  scanty.  Hands  and  feet 
were  generally  cold,  and  she  said  she  had  grown  nervous,  being 
easily  excited.  Pain  of  any  kind  was  trifling,  forming  a  marked 
contrast  to  most  of  the  cases  I  encounter. 

In  all  this  history  and  description  of  symptoms  there  was 
nothing  to  point  to  the  heart  outside  of  her  declaration  that  she 
sometimes  heard  a  queer  sound,  which  she  wanted  to  learn  the 
meaning  of.  The  pulse  was  85,  equal,  regular,  but  too  small  and 
weak.  The  broad,  strong  apex-beat  was  in  the  normal  situation, 
and  no  increase  of  either  superficial  or  deep  cardiac  dulness  could 
be  made  out.  However,  the  first  sound  was  partly  obscured  by  a 
loud,  rasping  murmur  that  was  audible  throughout  the  cardiac 
area  and  transmitted  around  the  left  side  to  the  lower  angle  of 
the  scapula.  The  pulmonary  second  sound  was  accentuated,  and 
in  the  dorsal  decubitus  a  softer  blowing  systolic  murmur  could 
be  heard  in  the  pulmonary  area.  Thinking  this  last  might  be  a 
chlorotic  murmur,  I  had  the  blood  examined,  and  found  that  the 
haemoglobin  was  reduced  to  65  per  cent,  red  and  white  cells  being 
normal  in  number. 

In  spite  of  the  absence  of  a  rheumatic  history  and  despite 
chlorosis,  there  seemed  no  good  reason  to  doubt  the  existence  of 
a  mitral  regurgitation  of  endocarditic  origin,  but  as  compensation 
was  preserved,  the  patient  was  reassured  as  to  the  harmlessness  of 
the  sound  she  had  noticed.  In  fact,  she  was  given  to  understand 
that  the  more  serious  conditions  were  the  blood-state  and  loss  of 
weight,  which  in  the  light  of  her  family  history  certainly  required 
attention.  She  was  given  a  little  strychnine  and  a  few  drops  of 
digitalis  to  improve  the  strength  of  her  pulse,  but  main  attention 
was  bestowed  upon  the  matter  of  nutrition.  Milk,  raw  eggs,  and 
fresh  air  were  insisted  upon.  The  patient  obeyed  instructions  to 
the  letter,  and  soon  was  disposing  admirably  of  two  quarts  of  milk 
and  ten  raw  eggs  daily  in  addition  to  three  good  meals.  Her  colour, 
weight,  and  general  condition  improved  steadily,  until  at  the  end 
of  two  months  she  looked  the  picture  of  health.    ISTevertheless,  the 


226  DISEASES  OF  THE   HEART 

murmur  persisted,  and  once  in  a  while  she  heard  that  same  endo- 
cardial soimd.  It  no  longer  worried  her,  however^  and  she  never 
complained  of  any  other  symptoms  referable  to  the  heart  or  dis- 
ordered circulation. 

In  this  case  it  would  be  difficult  to  say  how  much  the  mitral 
regurgitation  was  responsible  for  her  condition.  I  believe  the 
leak  was  so  slight  that  it  did  not  materially  affect  the  chylopoietic 
and  blood-making  organs,  but  that  the  state  of  her  general  health 
was  attributable  to  her  child-bearing  and  lactation,  which  in  a 
woman  with  hereditary  predisposition  to  pulmonary  tuberculosis 
proved  too  great  a  draught  on  her  vitality.  Had  she  been  allowed 
to  go  on  in  her  reduced  condition  she  would  in  time  have  devel- 
oped symptoms  either  of  cardiac  inadequacy  or  of  tuberculosis. 
As  it  is,  she  is  now  likely  to  remain  free  from  symptoms  of  valvu- 
lar disease  for  an  indefinite  time. 

I  have  notes  of  the  case  of  a  young  man  who,  because  of  a 
mitral  regurgitant  murmur  and  not  very  severe  symptoms  of  car- 
diac strain,  was  ordered  to  bed  by  his  physician,  and  there  re- 
mained for  two  years.  When  I  saw  him  he  had  mitral  insuffi- 
ciency sure  enough,  but  his  prolonged  rest  had  established  perfect 
compensation,  the  heart  being  not  demonstrably  enlarged  and  the 
liver  of  normal  size.  Yet  he  declared  he  could  not  get  up  or  stand, 
much  less  walk.  I  compelled  him  to  get  on  to  his  legs,  and  little 
by  little  to  walk  about,  with  the  result  that  he  found  he  could 
exercise  without  harm  or  symptoms  of  heart-weakness.  He  was 
easily  frightened  about  himself  for  two  or  three  years,  but  did  not 
manifest  dyspncr'a  or  other  cardiac  symptoms  even  when  riding  his 
wheel  over  hilly  and  sandy  roads.  The  last  time  he  was  seen  by 
me,  now  several  years  ago,  he  was  as  well  as  nine-tenths  of  the 
young  men  who,  like  him,  are  school-teachers.  At  the  most  he 
had  to  be  careful  of  his  stomach  and  guard  against  constipation. 

A  medical  student,  age<l  thirty-four,  sought  medical  opinion 
on  account  of  attacks  of  palpitation.  In  childhood  he  had  measles, 
pertussis,  and  chicken-pox,  and  dimly  recalled  having  had  a 
swollen  knee  when  five  years  old.  At  twelve  or  thirteen  was  so 
puny  and  frail  that  he  was  given  cod-liver  oil  and  kept  in  the 
house  during  the  winter,  but  after  fourteen  took  a  start  and  be- 
came rugged.  Fourteen  years  ago  he  had  gonorrhoea ;  had  used 
tobacco  from  the  age  of  seventeen.     In  1S03,  1804,  and  1895  he 


MITRAL  REGURGITATION 


227 


played  football  a  good  deal,  and  again  two  years  ago,  1898,  with- 
out any  distress  connected  with  his  heart,  excepting  on  one  occa- 
sion when,  after  ha\'ing  drunk  a  number  of  glasses  of  beer,  he 
played  in  a  very  rough  game.  lie  then  noticed  considerable  short- 
ness of  breath  and  several  times  had  to  drop  out  and  lie  down  on 
the  grass,  because  experiencing  great  difficulty  in  getting  breath. 
He  attributed  his  dyspnoea  to  the  fact  of  having  attempted  to  play 
on  a  full  stomach.  About  a  month  later  he  began  to  notice  his 
palpitations.  He  now  does  not  notice  dyspncea  except  on  running 
upstairs,  and  then  no  more  than  he  thinks  anybody  would  who 
was  soft  and  out  of  training.  In  spring  of  1900  he  consulted  me, 
but  nothing  positive  was  discovered  to  explain  his  palpitations, 
and  he  was  advised  to  give  up  his  tobacco.  This  he  did,  and  his 
palpitations  disappeared.  Upon  attempting  to  smoke  again  a  few 
months  subsequently  his  symptoms  returned  and  he  again  aban- 
doned his  smoking  permanently,  but  his  palpitations  still  con- 
tinued. 

Examination  of  his  urine  two  years  ago  showed  it  to  be  nor- 
mal. Last  spring  he  observed  for  the  first  time  that  a  prolonged 
and  severe  attack  of  palpita- 
tion was  followed  by  the  pas- 
sage of  a  large  amount  of  pale 


urine.  His  digestion  is  not 
good,  he  thinks,  there  being  a 
"  rumbling  and  roaring "  in 
the  bowels,  some  eructations, 
and  occasionally  heart-burn. 
Sometimes  his  flatulence  is 
followed  by  diarrhoea,  but  or- 
dinarily his  bowels  are  regu- 
lar. His  sleep  is  good  and  his 
habits  are  now  excellent. 

The  pulse  varies  much  in 
its  irregularity,  being  steady 
for  twenty  or  thirty  seconds, 
and    then    intermittine;    everv 


Fig.  36. — Relative  Dulness,  Case  of 
Mitral  Insufficiency. 


few  beats  ;  it  is  equal,  of  good  volume,  and  of  normal  rate.     There 
is  no  perceptible  cardiac  impulse  except  when  the  heart  gives  a 


more  than  usually  vigorous  contraction. 


Absolute  dulness  is  nor- 


228  DISEASES  OF   THE   HEART 

mal,  but  relative  diihiess  measures  1^  inclies  to  right  of  the  sternum 
and  4^  to  the  left  of  the  median  line  in  the  third  interspace  (Fig. 
36).  The  sounds  are  distinct,  but  the  pulmonic  second  markedlj' 
accentuated.  At  the  apex  and  round  about  the  nipple  there  is  a 
faint,  soft  systolic  murmur,  which  is  heard  distinctly  only  when 
the  heart  makes  a  strong  contraction  after  an  intermission.  In 
the  fifth  interspace,  within  the  left  nipple-line,  there  is  a  sugges- 
tion of  a  very  short  presystolic  murmur.  The  systolic  murmur 
is  increased  somewhat  in  the  recumbent  position. 

There  can  be  no  doubt  of  the  existence  of  a  mitral  leak,  but  it 
is  not  quite  clear  whether  it  is  of  rheumatic  origin  or  resulted 
from  a  degree  of  cardiac  overstrain  during  that  game  of  football, 
and  from  which  the  heart  has  not  recovered. 

The  effect  of  tobacco  and  emotional  excitement  on  this  patient 
is  interesting.  After  having  both  smoked  and  chewed  for  seven- 
teen years  he  has  at  length  been  compelled  to  abandon  its  use, 
because  it  now  invariably  induces  an  attack  of  palpitation,  which 
is  described  as  a  '*  fluttering."  He  notices  also  that  the  excitement 
attending  a  quiz  or  examination  in  class  will  set  his  heart  to  flut- 
tering. Also  an  attack  is  pretty  sure  to  come  on  about  an  hour 
and  a  half  after  a  meal,  whereas  if  he  misses  a  meal  the  palpita- 
tion does  not  occur  until  the  usual  length  of  time  has  elapsed  after 
the  next  meal.  This  individual  is  highly  nervous,  not  being  able 
to  keep  still,  continually  moving  a  hand  or  foot.  It  is  this  insta- 
bility of  the  nervous  system  that  accounts  for  the  readiness  with 
which  his  heart  responds  to  stimuli  that  do  not  disturb  cardiac 
action  in  most  individuals. 

In  contrast  thereto  is  the  patient's  statement  that  even  vigor- 
ous effort  does  not  produce  palj^itation  and  only  a  moderate  degree 
of  breathlessness.  Lastly,  he  is  not  conscious  of  the  linlutually 
intermittent  action  of  his  heart  when  he  is  at  rest. 

The  treatment  advised  was  a  blue  ]»ill  once  in  two  weeks,  to  be 
followed  by  a  dose  of  salts  next  morning,  tincture  of  fat-free  digi- 
talis in  5-drop  doses,  and  -^  of  strychnine  thrice  daily,  the  avoid- 
ance of  immoderate  physical  effort,  and  a  dietary  rich  in  proteids 
and  containing  a  restricted  amount  of  carbohydrates. 

Intense  cardiac  pain  of  the  kind  to  merit  the  term  angina 
pectoris  is  rare  in  mitral  regurgitation,  particularly  in  the  young, 
or  when  of  endoearditic  origin.     In  some,  however,  there  are  neu- 


MITRAL  REGURGITATION  229 

ralgic  pains  above  the  pra'cordiuni,  which,  by  reason  of  an  asso- 
ciated sense  of  oppression,  may  be  called  not  inaptly  anginoid 
pains.  The  pain  most  frequently  complained  of  by  these  patients 
is  a  left  inframammary  neuralgia,  which  is  variously  described, 
as  if  a  knife  were  being  thrust  through  the  heart,  or  as  if  the  pain 
would  take  the  breath  away,  or  as  if  the  heart  were  being  clutched 
or  twitched  or  screwed  together.  This  pain  is  apt  to  appear  sud- 
denly, to  be  sharp  and  lancinating,  to  last  a  few  seconds,  and  recur 
after  varying  intervals,  to  be  confined  to  the  prsecordia,  or  to  radi- 
ate around  the  back,  down  into  the  hypochondrium,  up  into  the 
neck,  or  even  into  the  left  arm.  Occasionally  the  cutting  pain 
subsides,  leaving  a  feeling  of  soreness  behind.  This  heart-pain,  as 
it  is  called,  is  not  angina  pectoris,  but  a  true  intercostal  neuralgia, 
and  is  very  apt  to  be  associated  with  palpitations.  For  this  reason 
the  patients  are  all  the  more  convinced  that  the  pain  is  in  the 
heart  itself.  I  have  known  strong  men,  and  even  physicians, 
dreadfully  alarmed  by  such  an  attack.  Its  association  with  cer- 
tain tender  areas  pointed  out  by  Head  indicate  its  origin  in  dis- 
orders of  indigestion,  and  hence  its  frequent  occurrence  in  patients 
with  mitral  disease.  It  is  not  to  be  supposed,  however,  that  it  is 
at  all  peculiar  to  this  class  of  cardiopaths. 

ISTot  long  ago  I  was  consulted  by  a  woman  of  thirty-six  on  ac- 
count of  a  sharp  pain  in  the  left  side  near  the  heart.  She  gave  a 
history  of  inflammatory  rheumatism  eighteen  years  before,  at 
which  time  she  was  ill  two  or  three  months.  She  remembered 
having  had  scarlatina  in  childhood,  followed  by  droj)sy  for  an  in- 
definite period.  She  had  had  two  attacks  of  measles,  once  in 
childhood,  and  again  at  the  age  of  twenty.  Thirteen  years  prior 
to  my  examination  she  had  suffered  from  la  grippe.  She  had  been 
married  sixteen  years,  given  birth  to  one  child,  and  for  many 
years  had  been  a  hard-working,  active  woman.  Her  chief  com- 
plaint was  a  sharp  pain  about  the  heart,  and  yet  in  response  to 
query  concerning  shortness  of  breath  said  that  when  she  ran  up- 
stairs, as  was  her  wont  in  order  to  get  up  quickly,  she  was  so  out 
of  breath  that  she  had  to  sit  down  to  recover  breath.  At  such 
times  she  also  became  blue.  Upon  rising  suddenly  she  felt  dizzy, 
her  hands  and  feet  swelled  sometimes,  was  annoyed  by  gas  in  the 
stomach  and  bowels,  and  had  a  poor  appetite.  Bowel  movements 
and   menses   were   regular,    though   the   last   were   scanty.      She 


230 


DISEASES  OP  THE  HEART 


sometimes  heard  a  grating  noise  that  seemed  to  come  from  the 
heart. 

Her  pulse,  while  sitting,  was  80,  small,  weak,  and  regular. 
The  apex-beat  in  the  fifth  left  interspace,  nipple-line,  was  weak, 
but  without  thrill.  Absolute  cardiac  dulness  was  normal,  but  rela- 
tive dulness  extended  to  the  sixth  costal  cartilage  below,  4  inches 
to  the  left  of  midsternum,  not  increased  to  right  (Fig.  37).     The 

first  sound  at  the  apex  was 
feeble,  being  partially  ob- 
scured by  a  murmur  and  suc- 
ceeded by  a  feeble  second  tone, 
while  the  pulmonic  second  was 
distinctly  accentuated.  All 
over  the  cardiac  area  was  a 
loud,  sawing  murmur  of  sys- 
tolic rhythm,  most  distinct  at 
the  apex,  and  transmitted 
around  the  left  side  to  the 
back.  The  liver  was  barely 
palpable,  yet  tender  in  the  re- 
gion of  the  gall-bladder,  but  in 
other  respects  the  abdomen 
was  negative.  The  condition 
was  plainly  a  mitral  regurgi- 
tation of  rheumatic  origin, 
with  imperfect  compensation  because  of  the  daily  strain  to  which 
the  heart  was  subjected. 

This  case  is  interesting  because  of  the  fact  that  although  the 
patient  admitted  dyspna-a  and  cyanosis  upon  unusual  physical 
effort,  she  was  yet  chiefly  disturbed  by  the  prircordial  pain.  This 
was  undoubtedly  an  intercostal  neuralgia  that  was  in  reality  due 
to  her  gastric  and  intestinal  fermentation  and  only  indirectly  to 
the  valvular  lesion. 

The  only  symptom  of  which  one  of  my  male  patients  com- 
plains is  an  intermittent  pulse  that  annoys  him  whenever  he 
breaks  away  from  his  strict  diet  or  confines  himself  too  closely 
to  his  office.  He  is  always  benefited  b}'  outdoor  exercise,  particu- 
larly fishing,  and  declares  he  has  no  shortness  of  breath  and  no 
uncomfortable  palpitation  unless  his  exercise  is  too  violent.     An- 


FiG.  -.V  /in  \-i;i-,A'i  AMI  L  I  !  ■  1 1  ■•  L  Dul- 
ness, Case  of  Mitkal  Kegurgitatiom 
(p.  229). 


MITRAL  REGURGITATION  231 

other  patient,  who  has  pronounced  yet  perfectly  compensated 
mitral  regurgitation,  is  able  to  endure  any  form  of  exercise,  even 
running,  without  any  other  symptom  than  a  rapid,  strong  heart- 
action  ;  while  still  a  third  bears  without  any  apparently  injurious 
effect  broadsword  practice  and  sparring. 

Between  such  cases  as  these  and  those  in  the  last  stages  of 
cardiac  incompetence  there  are  all  grades  of  sufferers.  In  what 
may  be  called  an  intermediate  stage — that  is,  when  compensation 
is  no  longer  complete — the  symptom  most  commonly  experienced 
is  dyspnoea.  Some  patients  do  not  notice  this  breathlessness  dur- 
ing ordinary  walking,  but  only  when  they  hurry  or  ascend  stairs 
rapidly.  Even  then  they  sometimes  say  in  response  to  queries 
concerning  their  ability  to  endure  exercise,  they  do  not  think  they 
get  any  more  out  of  breath  than  does  anybody  in  hurrying  up- 
stairs. The  fact  is,  such  persons  have  been  so  accustomed  to 
breathlessness,  even  for  years  perhaps,  that  they  do  not  attach 
any  importance  to  it,  and  do  not  consider  it  a  symptom  of  heart- 
weakness.  Indeed,  so  long  as  dyspnoea  is  not  more  pronounced, 
the  mitral  lesion  may  be  considered  in  a  state  of  fair  though  not 
perfect  compensation. 

In  this  intermediate  stage  there  is  a  degree  of  chronic  pulmo- 
nary congestion  which  renders  these  patients  particularly  liable 
to  coughs  and  colds.  These  may  be  transient  and  troublesome  only 
during  damp,  cold  weather,  disappearing  altogether  in  summer, 
but  in  not  a  few  cases  there  is  a  very  obstinate  chronic  bronchitis. 
When  this  last  is  present,  it  possesses  no  peculiar  features  that 
distinguish  it  from  the  chronic  bronchial  catarrh  so  often  observed 
in  persons  without  valvular  disease.  It  has  been  my  experience, 
however,  that  a  persistent  and  frequent  cough  is  very  apt  to  inten- 
sify the  already  existing  dyspnoea  by  reason  of  the  strain  it  puts 
upon  the  right  ventricle.  Consequently,  whenever  cough  makes 
its  appearance  in  a  case  of  mitral  regurgitation  it  is  not  to  be  re- 
garded as  of  no  importance  and  likely  to  "  wear  oif."  It  may 
gradually  wear  away  if  the  season  is  propitious,  but  it  is  far  more 
likely  to  run  on  into  a  chronic  condition.  It  should  be  borne  in 
mind,  also,  that  in  these  mitral  patients  cough  may  be  attended 
by  blood-spitting  from  rupture  of  a  congested  capillary  in  the 
bronchial  mucosa,  and  is  not  at  all  significant  of  tuberculosis.  Oc- 
casionally cough  is  induced  by  unusual  exertion  or  excitement,  and 


232  DISEASES  OF   THE   HEART 

is,  of  course,  due  to  the  irritation  of  excessive  pulmonary  hjper- 
aemia.  In  two  instances  coming  under  my  notice  it  was  attended 
by  a  profuse  serous  frothy  expectoration  that  betokened  acute 
(X'dema  of  the  lungs.  In  both  these  cases  the  attack  subsided  with- 
out treatment  after  the  patients  had  betaken  themselves  to  absolute 
physical  repose.  Such  attacks  are  not  without  danger,  and  often 
necessitate  energetic  treatment. 

The  following  case  is  an  example  of  the  occurrence  of  haemop- 
tysis in  mitral  regurgitation.  In  March,  1901,  a  tall,  slender 
girl  of  nine  was  brought  to  me  by  her  parents,  who  were  in  a  state 
of  great  alarm  because  of  her  having  spit  up  a  little  blood  a  few 
days  previously.  One  of  the  child's  maternal  uncles  was  in  Colo- 
rado on  account  of  his  lungs,  and  consequently  it  was  feared  the 
little  patient  might  be  developing  pulmonary  tuberculosis.  It 
was  ascertained  that  there  had  been  no  antecedent  cough,  but  that 
the  haemoptysis,  which  had  occurred  more  than  once,  had  followed 
upon  rather  more  than  the  usual  amount  of  running.  There  was  a 
history  of  measles,  but  not  of  scarlet  fever  and  not  of  rheumatism, 
although  the  child  had  in  earlier  years  suffered  a  good  deal  from 
pains  in  her  legs,  and  been  wont  to  cry  out  in  her  sleep  from  night 
terrors.  Upon  examination  I  readily  discovered  a  loud,  blowing 
systolic  apex-murmur  that  was  propagated  to  the  back.  The  heart 
was  unmistakably  enlarged  and  the  liver  was  palpable.  As  a  re- 
sult of  these  findings  and  in  the  light  of  the  history  I  had  no  hesi- 
tation in  pronouncing  the  case  one  of  mitral  regurgitation,  prob- 
ably of  rheumatic  origin,  and  also  in  explaining  to  the  parents 
that  the  symptom  causing  their  alarm  did  not  denote  tuberculosis. 
They  were  told  that  it  was  the  result  of  congestion  of  the  lungs 
brought  on  by  a  degree  of  physical  effort  that  was  too  much  for 
her  damaged  heart.  It  may  be  added  that  the  knowledge  of  their 
child's  valvular  lesion  did  not  serve  to  allay  their  apprehension. 
This  case  also  illustrates  how  remarkably  unconscious  of  dyspnopa 
children  often  are  who  have  mitral  insuffieioncv,  for  this  child 
not  only  was  fond  of  running  and  playing  hard,  but  said  such 
sports  did  not  make  her  feel  bad  or  get  out  of  breath. 

In  cases  of  imperfect  coinpeiisation  there  are  likely  to  be  symp- 
toms of  stasis  within  the  vessels  of  the  abdomen  as  well  as  of  the 
lungs.  Disorders  of  appetite  and  digestion  are  now  quite  com- 
mon.    Some  patients  lose  tlioir  a])pctite  altogether,  or  if  they  feel 


MITRAL   REGURGITATION  233 

hungry  when  sitting  down  to  eat,  soon  find  themselves  full  and 
uncomfortable,  not  because  of  having  taken  too  much,  but  on  ac- 
count of  the  formation  of  gas  that  distends  the  stomach  and  pro- 
duces a  sense  of  repletion  with,  in  some  cases,  an  intensification  of 
the  already  existing  dyspnoea.  These  patients  declare  they  bloat  up 
after  meals,  and  often  complain  of  annoying  eructations.  The 
escaping  gas  is  either  tasteless  and  odourless  or  tastes  strongly  of 
some  of  the  ingesta.  Others  suffer  from  acid  indigestion,  pyrosis, 
burning  or  gnawing  in  the  pit  of  the  stomach,  colicky  pains,  etc. 
Some  patients  are  constipated  and  annoyed  by  flatulency,  while 
others  have  a  tendency  to  diarrhoea,  particularly  in  the  morning  be- 
fore breakfast.  In  a  few  instances  I  have  known  a  veritable  bu- 
limia, which  it  seemed  to  me  might  reasonably  be  attributed  to  the 
irritation  of  fatty  acids  and  gases.  It  is  not  uncommon  for  these 
patients  to  be  tormented  by  thirst,  which,  compelling  them  to  drink 
largely  and  often  of  cold  water,  aggravates  their  trouble.  The  con- 
dition of  chronic  gastric  catarrh  responsible  for  these  symptoms  is 
not  peculiar  to  mitral  patients;  it  is  only  one  of  the  many  manifes- 
tations of  secondary  visceral  congestion  which  bring  the  patients  to 
the  physician.  The  digestive  defect  is  often  the  result  of  dietetic 
indiscretions,  yet  their  mitral  leak  predisposes  them  to  suffer  from 
errors  in  diet  which  would  not  affect  them  were  they  healthy. 

In  females  chronic  hyperemia  of  the  pelvic  organs  is  shown  by 
leucorrhoea  and  menstrual  derangements.  In  some  menstruation 
is  profuse  and  irregular,  while  in  others  again  the  catamenia  are 
scanty  or  suppressed. 

Stasis  in  the  ha?morrhoidal  plexuses  may  lead  to  piles  and  con- 
sequent constipation.  Renal  congestion  is  shown  by  scanty,  light- 
coloured  urine,  rich  in  urates.  Albumin  and  casts  do  not  appear 
as  a  rule  until  in  the  latter  stage  of  the  valvular  disease,  when 
dropsy  has  come  on. 

Examination  of  the  liver  in  this  intermediate  stage  of  de- 
fective compensation  may  or  may  not  disclose  enlargement  of  the 
organ.  In  most  instances  hepatic  dulness  is  found  to  reach  a 
finger's  breadth  or  so  below  the  inferior  margin  of  the  ribs,  while 
the  lower  border  of  the  organ  feels  smooth,  rounded,  and  firm. 
Palpation  may  also  disclose  more  or  less  tenderness  of  the  organ, 
so  that  the  patient  winces  and  involuntarily  resists  further  pal- 
pation. If  the  congestion  has  affected  the  biliary  passages  and 
17 


234  DISEASES  OF   THE   HEART 

led  to  their  catarrhal  occlusion,  more  or  less  complete,  this  may  be 
showu  by  icterus.  As  a  rule  this  is  slight,  and  combined  with 
capillary  congestion  produces  a  muddy  hue  of  the  face. 

In  the  most  of  these  cases  of  partially  destroyed  compensation 
there  is  not  actual  cyanosis,  but  instead  the  lips  and  cheeks  present 
a  dark-red  colour  that  by  the  uninitiated  is  very  apt  to  be  mistaken 
for  an  appearance  of  ruddy  health.  If  the  hands  and  arms  are 
inspected  their  superficial  veins  are  seen  to  stand  forth  too  promi- 
nently, while  by  night  the  ankles  display,  if  not  actual  pitting,  at 
least  a  degree  of  puffiness  and  tension  which  is  but  a  little  way 
removed  from  a'dema  and  betokens  marked  capillar}-  stasis. 

The  patients  now  find  their  breath  uncomfortably  short  on 
hurry,  and  even  when  they  walk  leisurely  they  are  conscious  of 
slight  breathlessness.  In  addition,  they  notice  a  feeling  of  fulness 
or  tightness  in  the  heart-region,  which  if  not  actually  painful  is 
very  akin  to  pain.  They  find  also  that  they  become  fatigued  more 
easily  than  formerly,  and  that  talking  requires  more  effort  than 
is  quite  comfortable,  while  if  they  converse  during  walking  they 
pant  noticeably.  Efforts  before  endured  without  conscious  effect 
now  throw  them  into  perspiration,  and  make  them  glad  to  sit  or 
perhaps  lie  down  and  rest.  Such  symptoms  constitute  the  earliest 
evidence  of  cardiac  inadequacy,  and  if  not  heeded  will  go  on  to 
symptoms  of  positive  loss  of  compensation. 

In  some  persons  in  this  stage  there  is  marked  tendency  to 
drowsiness  after  meals  or  whenever  they  sit  quiet  and  strive  to  fix 
their  attention  on  a  speaker.  This  is  especially  noticeable  if  the 
atmosphere  is  close  and  hot.  Some  persons  find  the  heat  and 
closeness  produce  a  feeling  of  faintness  or  suffocation  which  neces- 
sitates their  seeking  the  open  air.  Sleep  is  heavy,  with  frightful 
dreams,  or  there  is  insomnia,  so  that  in  the  morning  the  patients 
are  intensely  weary  and  unrefreshed.  Headaches  are  not  uncom- 
mon in  this  stage,  and  for  the  most  part  are  dull  frontal  pains 
accompanied  by  a  sense  of  mental  weariness  and  confusion. 

A  still  more  advanced  stage  of  lost  compensation  is  shown  by 
a  young  lady  with  free  mitral  regurgitation  and  adherent  peri- 
cardium whom  T  have  under  (»l)servation  at  this  present  writing. 
The  skin  along  the  shaft  of  each  tibia  can  be  indented  slightly  by 
firm  pressure;  the  external  jugulars  stand  forth  as  large  as  my 
little  finger,  are  painful,  and  show  the  positive  venous  pulse  of 


MITRAL   REGURGITATION  235 

tricuspid  leakage ;  the  waist  looks  and  feels  disproportionately 
large,  while  below  the  ribs  the  big  resisting  liver  extends  to  the 
level  of  the  umbilicus,  causing  the  abdomen  at  its  upper  zone  to 
stand  out  unnaturally ;  the  veins  on  the  hands  and  arms  are 
turgid,  while  the  pulse  is  small,  weak,  and  faltering,  but  not  much 
accelerated,  seldom  reaching  100.  Examination  shows  a  diffused 
unsteady  impulse  throughout  the  pr^ecordium,  while  the  broad, 
rather  strong,  immovably  fixed  apex-beat  is  in  the  sixth  inter- 
space, almost  to  the  left  anterior  axillary  line;  absolute  cardiac 
dulness  is  so  enormously  increased  both  by  reason  of  dilatation 
and  the  retraction  of  the  lung-borders,  as  to  nearly  correspond 
with  relative  dulness.  All  over  the  left  chest  can  be  heard  an  in- 
tense systolic  murmur,  which  is  unmistakably  a  mitral  regurgitant 
one,  while  to  the  right  of  the  lower  portion  of  the  sternum  is  a 
somewhat  softer  systolic  bruit  that  is  probably  tricuspid.  The 
scanty  urine  contains  6  per  cent  of  albumin,  hyaline  and  granular 
casts,  while  menses  have  been  absent  for  the  last  six  months.  In 
the  way  of  subjective  symptoms  there  are  the  following:  Short- 
ness of  breath  when  walking  or  conversing,  an  occasional  short, 
dry  cough,  pain  in  the  distended  jugulars,  when  these  are  unusu- 
ally full,  a  sensation  of  fulness  and  tightness  in  the  region  of  the 
liver,  at  times  an  intense  uncontrollable  nervousness  and  restless- 
ness, but  almost  no  sense  of  digestive  discomfort,  and  the  appetite 
is  remarkably  good. 

This  patient's  first  breakdown  occurred  ten  years  ago,  and  has 
been  followed  by  two  or  three  others.  This  present  manifesta- 
tion of  ruptured  compensation  began  six  months  ago,  and  for  sev- 
eral months  was  so  bad  that  she  had  ascites,  dropsy  of  the  ankles, 
and  was  confined  to  her  apartment.  She  was  not  then  under  my 
care,  but  was  at  her  home  in  an  adjoining  State.  In  this  case 
there  are  to  me  two  features  of  particular  interest:  (1)  The  com- 
plication of  pericardial  adhesions,  which  utterly  preclude  the  pos- 
sibility of  reducing  the  dilatation  of  the  left  ventricle  by  which 
the  regurgitation  is  intensified,  and  (2)  the  absence  of  dropsy, 
although  the  tricuspid-valve  is  incompetent.  Compensation  is  de- 
stroyed, and  I  fear  irretrievably  so,  but  the  disturbance  of  circu- 
lation has  not  yet  reached  the  degree  nor  produced  the  distressing 
subjective  symptoms  sometimes  witnessed  in  cases  of  mitral  re- 
gurgitation. 


236  DISEASES   OF   THE   HEART 

When  in  this  disease  compensation  is  wholly  gone,  there  is  a 
marked  aggravation  of  all  the  objective  and  subjective  symptoms 
that  have  been  described.  There  are  now  evidences  of  extreme 
stasis.  Dropsy  is  generally  a  pronounced  feature,  and  in  many 
cases  dominates  the  scene.  Beginning  at  the  ankles,  it  creeps 
upward  until  it  involves  the  integument  of  the  trunk,  and  it  may 
be  of  the  upper  extremities.  There  is  also  in  this  stage  transuda- 
tion into  the  serous  cavities,  ascites,  hydrothorax,  and  pulmonary 
oedema.  This  condition  leads  to  orthopncea,  cough,  and  frothy  or 
even  bloody  sputum.  I  recall  a  feuuile  who  in  this  condition  of 
hopeless  suffering  was  sitting  on  her  bed,  supporting  her  elbows  on 
her  knees  and  her  face  in  her  hands,  and  was  coughing  pure  blood. 
She  had  been  in  this  plight  for  days  and  had  abandoned  hope,  hav- 
ing been  told  by  more  than  one  doctor  that  her  condition  was  hope- 
less. Three  months  thereafter  she  was  walking  about  the  house 
free  from  oedema.  This  case  is  described  more  fully  in  the  chapter 
on  Treatment.  Another  female  patient  who  now  visits  my  office 
was,  four  years  ago,  so  dropsical  that  she  appeared  water-logged, 
and  for  six  weeks  had  been  obliged  to  get  what  sleep  she  could  in 
an  easy  chair  and  resting  her  arms  on  a  table  in  front  of  her. 

When  stasis  reaches  such  an  extreme  degree  it  has  generally 
been  preceded  by  dilatation  of  the  right  ventricle  and  signs  of  rel- 
ative tricuspid  insufficiency.  This  condition  of  the  right  heart 
may  and  usually  does  precede  the  dropsy,  but  oedema  presents  such 
differences  in  extent  and  time  of  appearance  that  something  more 
than  mere  stasis  is  required  for  its  production.  Accordingly,  it  is 
now  believed  that  serous  transudation  takes  place  when  the  capil- 
lary walls  become  abnormally  permeable  or  there  is  a  state  of 
hydra'uiia.  In  some  cases  doubtless  the  kidneys  have  lost  their 
ability  to  eliminate  the  sodium  chloride  of  the  blood  the  same  as 
in  nephritis.  In  this  event  the  oedema  is  soft  and  pits  far  more 
easily  than  when  mechanical  interference  witli  the  circulation  is 
the  chief  factor. 

In  some  cases  dropsy  becomes  so  excessive  that  the  skin  of  the 
legs  becomes  red  and  shining,  or  even  forms  blobs,  which,  l)nrsting, 
permit  the  serum  to  ooze  forth,  and  tluis  diminish  the  tension  of 
the  surrounding  ])arts.  Under  such  circumstances  the  nutrition  of 
the  integument  becomes  so  impaired  and  infection  is  so  easy  that 
a  simple  srratcli  nr  abrasion  may  set  up  inllninnuition. 


MITRAL  REGURGITATION  237 

In  this  stage  of  things  extreme  gastro-intestinal  congestion 
and  abdominal  distention  from  fluid  and  flatus  prevent  the  taking 
of  adequate  nourishment.  Cerebral  congestion  and  oedema  pro- 
duce headache,  insomnia,  or  somnolence,  an  unreasonable  fret- 
fulness  and  irritability,  or  a  low,  muttering  delirium.  The  pa- 
tient's condition  is  now  one  of  indescribable  and  unendurable  suf- 
fering, so  that  physician  and  friends  alike  breathe  a  sigh  of  relief 
when,  after  weeks  or  months  of  such  hardship,  death  ends  the 
struggle. 

It  only  remains  to  say  a  word  concerning  those  cases  of  mitral 
regurgitation  which  are  either  complicated  by  chronic  nephritis 
or  are  secondary  to  the  dilatation  of  the  left  ventricle  consequent 
upon  the  Bright's  disease.  These  cases  do  not  differ  essentially 
from  those  of  the  class  just  considered.  There  is,  however,  an  ele- 
ment of  uraemia  in  these  cases  which  is  apt  to  modify  the  picture 
somewhat.  These  patients  are  apt  to  suffer  from  a  form  of  dysp- 
noea that  is  very  distressing  and  difficult  to  relieve  by  treatment. 
It  consists  of  sudden  paroxysms  or  intensifications  of  their  ha- 
bitual shortness  of  breath  which  come  on  independently  of  exer- 
tion or  any  other  exciting  cause.  These  may  be  worse  at  night — 
are  so  generally,  but  are  not  necessarily  so,  for  I  have  known 
them  to  occur  by  day.  They  have  always  seemed  to  me  to  be  of 
toxic  origin  or  to  be  partly  renal  and  partly  cardiac.  Headache 
and  nausea  are  also  likely  to  torment  the  patient,  and  inflamma- 
tions of  the  serous  membranes  are  not  uncommon.  Dropsy  is 
often  very  pronounced,  and  is  peculiarly  soft  and  rebellious  to 
treatment.  In  other  cases  pulmonary  and  cerebral  symptoms  pre- 
dominate. They  all  furnish  an  absolutely  unfavourable  prognosis 
on  account  of  the  associated  or  antecedent  kidney  lesion. 

Paroxysms  of  dyspnoea,  sufiicient  to  be  termed  cardiac  asthma, 
are  not  very  common  in  mitral  incompetence,  unless  some  compli- 
cation, such  as  chronic  nephritis,  is  present,  to  which  the  regurgi- 
tation is  sometimes  secondary.  In  these  latter  cases  asthmatic 
seizures  are  frequent,  or  the  dyspnoea  assumes  the  Cheyne-Stokes 
type.  Likewise,  other  sjmiptoms  properly  belonging  to  mitral 
regurgitation  may,  when  associated  with  chronic  nephritis,  be 
modified  by  ura?mic  manifestations.  There  may  be  very  distress- 
ing nausea  and  vomiting,  and  the  physician  may  be  at  a  loss  to 
know  whether  the  symptoms  be  due  to  renal  inadequacy,  or  to 


238  DISEASES  OF   THE   HEART 

passive  congestion  of  the  stomach  depending  upon  the  regurgi- 
tation. 

If  in  a  given  case  of  mitral  regurgitation  ascites  appears 
prior  to  or  independent  of  anasarca,  it  is  due  to  some  compli- 
cation, and  in  my  experience  this  has  most  frequently  proved  to 
be  adherent  pericardium.  These  are  the  cases  sometimes  de- 
scribed as  pseudo-atrophic  cirrhosis  of  the  liver. 

Embolism  from  the  detachment  of  a  vegetation  is  not  common 
in  mitral  insufficiency  unless  it  be  complicated  with  acute  endo- 
carditis, yet  this  untoward  event  may  occur,  and  then  produces 
symptoms  depending  upon  the  organ  in  which  the  embolus  is 
arrested.  If  this  be  the  kidney,  there  is  likely  to  be  bloody  urine, 
and  yet  it  is  not  uncommon  to  discover  post-mortem  evidences  of 
infarcts  produced  by  emboli  of  such  minute  size  as  to  have  escaped 
detection  during  life. 

Cerebral  embolism  produces  symptoms,  too  characteristic  to 
escape  notice.  As  the  left  middle  cerebral  artery  is  the  one  most 
commonly  plugged,  it  is  followed  by  aphasia  and  right-sided  hemi- 
plegia. An  embolus  entering  the  hepatic  artery  produces  acute 
icterus  and  symptoms  closely  resembling  acute  yellow  atrophy  of 
the  liver.  In  the  case  of  the  spleen,  the  sudden,  sharp  pain 
is  likely  to  l)e  followed  by  tenderness  and  enlargement  of  the 
organ.  If  an  artery  of  one  of  the  extremities  is  thus  occluded, 
characteristic  pain  is  followed  by  loss  of  pulsation  in  the  artery 
below  the  seat  of  embolism,  by  weakness,  numbness,  coldness,  and 
paresthesia,  and  even  by  gangrene  of  the  limb,  if  the  main  artery 
happens  to  be  plugged.  Usually,  however,  these  symptoms  grad- 
ually disajipear  with  the  establishment  of  adequate  collateral  cir- 
culation. A  by  no  means  uncommon  effect  of  the  terminal  stage 
of  mitral  regurgitation  is  the  occurrence  of  pulmonary  infarcts 
due  to  the  lodgment  in  the  pulmonary  capillaries  of  minute  frag- 
ments of  thrombi  that  have  formed  in  the  dilated  right  chambers 
of  the  heart.  Pain  in  the  affected  lung  may  or  may  not  be  felt,  but 
if  the  patient  suddenly  begins  to  cough  up  clear  l)lood  it  is  very 
suspicious  of  j)uhMonary  infarction. 

Very  exceptionally,  a  mass  of  considerable  size  may  be  swept 
off  from  the  cardiac  thrombus,  and  entering  the  pulmonary  artery 
or  one  of  its  large  branches,  may  produce  instantaneous  dyspncx^a 
and  speedy  death. 


MITRAL  REGURaiTATION  239 

Physical  Signs. — Inspection. — There  is  nothing  in  the  ap- 
pearance of  individuals  with  a  latent  mitral  insufficiency  to  sug- 
gest the  existence  of  their  disease.  In  some  instances  capillary  con^ 
gestion  is  just  sufficient  to  impart  to  the  lips  and  cheeks  a  slightly 
heightened  colour  that  is  easily  mistaken  for  the  hue  of  health ; 
it  is,  however,  deeper  than  the  rosy  glow  of  perfect  circulation. 
In  a  still  more  advanced  degree  of  congestion  the  lips  become  of  a 
Muish  or  even  purplish  colour,  the  capillaries  of  the  face  are  in- 
jected, and  the  fingers  also  display  more  or  less  cyanosis.  There 
is,  however,  nothing  in  this  appearance  to  indicate  more  than  im- 
peded circulation,  and  hence  it  is  not  peculiar  to  mitral  regurgi- 
tation. 

In  children  with  long-standing  mitral  disease  the  fingers  are 
apt  to  be  clubbed,  the  stature  stunted,  the  shoulders  stooping,  and 
the  preecordium  bulging.  In  adults,  on  the  other  hand,  inspection 
of  the  cardiac  area  reveals  no  alteration  of  the  kind  seen  in 
children. 

The  apex  may  be  displaced  somewhat  to  the  left,  depending  on 
the  degree  of  left-ventricle  hypertrophy,  and  if  serious  dilatation 
is  not  present  is  broader  and  stronger  than  in  health.  If  the  right 
ventricle  is  also  sufficiently  enlarged  to  lie  well  down  in  the  sulcus 
formed  by  the  union  of  the  diaphragm  with  the  anterior  chest- 
wall,  its  pulsations  are  seen  more  or  less  distinctly  directly  below 
the  ensiform  appendix.  This  epigastric  pulsation  forms  an  im- 
portant sign  of  right-ventricle  hypertrophy,  and  hence  is  a  second- 
ary sign  of  mitral  disease.  It  should  be  carefully  distinguished 
from  the  throbbing  of  the  abdominal  aorta,  so  often  observed  in 
this  situation  in  neurotic  individuals  with  thin  abdominal  parietes. 
Of  course  the  information  to  be  derived  from  inspection  depends 
largely  upon  the  condition  of  the  thoracic  walls,  and  hence  in- 
spection is  of  greatest  value  in  persons  whose  hearts  are  dispro- 
portionately large  as  compared  with  the  size  of  the  chest. 

Palpation. — In  compensated  and  uncomplicated  mitral  regur- 
gitation the  pulse  possesses  no  distinctive  characters  aside  from  its 
lowness  of  tension.  Its  rate  is  usuall}^  somewhat  accelerated,  its 
tension  low,  and  in  compensated  cases  at  least,  it  is  regular  in  fre- 
quency, force,  and  volume.  As  the  energy  of  the  heart  wanes,  as 
its  walls  become  degenerated  and  its  auricles  dilated,  the  pulse 
grows  strikingly  irregular  and  intermittent,  the  pulse-waves  dif- 


24U  DISEASES  OF  THE  HEART 

fering  from  each  other  in  size  and  strength,  coming  at  uneven  dis- 
tances, and  often  dropping  out  altogether  even  when  the  heart- 
beats are  not  themselves  intermittent  (Fig.  38).  Such  a  pulse  is 
exceedingly  difficult  to  count,  and  if  subjected  to  a  little  pressure 
b}'  the  finger,  for  the  purpose  of  having  its  characters  brought 


Fig.  38. — Sphyqmogkam  of  Case  of  Mitral  Kegukgitation,  showing 

Irregularity  of  Pulse. 

(Personal  observation.)     Enlarged. 

out  more  distinctly,  it  disappears  from  beneath  the  palpating 
finger  in  a  manner  that  makes  it  very  elusive.  This  extreme 
irregularity  of  the  pulse  is  most  fre(]uent  when  regurgitation  is 
combined  with  stenosis  or  an  adherent  pericardium. 

The  pulse  in  the  two  wrists  is  generally  equal,  but  cases  have 
been  described  in  which  the  right  was  distinctly  smaller  than  the 
left,  owing  to  relative  tricuspid  insufficiency  and  consequent  pres- 
sure of  the  dilated  right  auricle  on  the  subclavian  artery.  Balfour 
states  that  if  the  arm  is  elevated  the  peculiar  characters  of  the 
pulse — i.  e.,  its  irregularity  and  lowiie.ss  of  tcii.sion — are  brought 
out  more  distinctly. 

Palpation  of  the  pra'cordia  confirms  the  information  obtained 
by  the  eye,  but  in  addition  enables  one  to  better  api)reciate  the 
strength  of  cardiac  contractions.  It  may  also  detect  thrill  or  pul- 
sations that  cannot  be  perceived  by  inspection.  Palpation  is  often 
a  valuable  means  of  ascertaining  the  size  of  the  heart,  particularly 
in  females  in  whom  excessive  mammary  development  may  prevent 
accurate  percussion.  By  pressing  the  fingers  gently  yet  firmly 
into  the  intercostal  spaces  beneath  the  breast  one  can  ascertain  the 
position  of  tlic  a])('X-beat,  and  thus  judge  of  ^he  size  of  the  left 
ventricle. 

Authorities  differ  as  regards  the  existence  of  a  thrill  at  the 
apex  in  cases  of  pure  and  uncomplicated  mitral  regurgitation. 
When,  however,  suoh  a  thrill  is  present  it  is  systolic,  and  felt 


MITRAL  REGURGITATION 


241 


witli  greatest  intensity  at  the  immediate  seat  of  apex-impulse, 
since  it  is  the  palpable  expression  of  the  murmur.  For  my  part  I 
am  perfectly  sure  of  its  occasional  existence  in  cases  without  con- 
joined mitral  stenosis. 

Lastly,  by  palpation  of  the  epigastric  notch  one  can  also  judge 
of  the  degree  of  compensatory  enlargement  and  vigour  of  the  right 
ventricle.  In  this  way  one  can  often  determine  that  the  ventricle 
is  hypertrophied,  when  for  one  reason  or  another  it  is  difficult  or 
impossible  to  outline  the  chamber  by  percussion. 

Percussion. — This  means  of  cardiac  examination  should  never 
be  neglected,  since  as  a  general  thing  it  furnishes  the  most  valu- 
able and  reliable  information  concerning  the  heart's  condition. 
Indeed,  percussion  is  almost  our  only  means  of  ascertaining  the 
size  and  shape  of  the  heart,  and  hence  of  learning  what  and  how 
extensive  have  been  the  secondary  changes  wrought  by  the  valvular 
defect.  If  in  the  lesion  now 
under  consideration  percus- 
sion does  not  detect  increase 
of  absolute  or  relative  dulness 
to  the  right  and  downward, 
the  inference  is  warranted, 
even  though  there  be  an  in- 
tense systolic  bruit,  that  the 
leak  is  not  free,  or  that  being 
free  it  has  nevertheless  been 
perfectly  compensated.  In 
most  cases  of  mitral  regurgi- 
tation, however,  the  lesion 
has  led  to  enlargement  of  the 
right  ventricle,  and  in  such  an 
event,  deep-seated  if  not  super- 
ficial dulness  is  increased  to 
the  right  and  inf eriorly ;  and  hence  the  extent  to  which  dulness  is 
increased  is  a  criterion  by  which  we  can  judge  of  the  freedom  of 
the  leak  or  of  the  compensation.  Secondary  enlargement  of  the 
left  ventricle  is  shown  by  increased  dulness  of  the  left  (Fig.  39). 

Mitral  regurgitation,  it  will  be  remembered,  leads  to  dilata- 
tion of  the  left  auricle  as  well  as  hypertrophy;  hence  in  pro- 
nounced cases  the  outline  of  the  deep  cardiac  dulness  at  its  upper 


Fig.  39. — Relati%'e  Dulness  in  a  Typical 
Case  of  Mitral  Eegurgitation. 


242 


DISEASES  OF  THE   HEART 


and  outer  corner,  so  to  speak,  is  broad  and  rounded,  corresponding 
to  the  enlargement  of  the  auricle.  It  is  not  always  easy  to  deter- 
mine this  alteration  of  shape  by  percussion ;  yet  if  firm,  percus- 
sion is  made,  and  the  chest-wall  is  thin  and  yielding,  it  is  some- 
times possible  to  determine  the  extent  to  which  the  left  auricle  has 
been  affected  by  the  regurgitation. 

Auscultation. — This  forms  a  very  valuable  means  of  cardiac 
examination,  for  without  the  information  thus  obtained  one  can- 
not safely  assert  that  mitral  regurgitation  does  or  does  not  exist. 
It  sliould  not  be  relied  upon  to  the  exclusion  of  other  methods  of 
investigation,  however,  for  reasons  that  will  be  stated  presently. 
The  auscultatory  evidence  of  valvular  disease  lies  in  certain  acous- 
tic phenomena  which  are  produced  by  soniferous  currents  in  the 
blood-stream,  and  are  called  murmurs.  It  is  plain  that  many  dif- 
ferent factors  influence  the  character  of  a  murmur,  and  that  if 
reliable  information  is  to  be  derived  from  the  study  of  a  murmur 

the  characters  peculiar  to  each 
must  be  understood. 

The  auscultatory  indica- 
tion of  mitral  regurgitation, 
then,  is  a  systolic  murmur 
heard  with  maximum  inten- 
sity in  the  mitral  area — i.  e., 
at  or  close  to  the  apex-beat 
(Fig.  40).  Such  a  bruit  is 
not,  however,  an  invariable 
sign  of  mitral  incompetence, 
since  it  may  be  accidental, 
and  hence  there  are  other 
facts  concerning  a  mitral  re- 
gurgitant murmur  which  must 
l)e  understood. 

The  murmur  is  systolic  be- 
cause produced  during  the  con- 
tracti(.M  of  the  ventricles,  and  therefore  it  is  strictly  synchronous 
with  the  first  sound,  althougli  it  not  infrequently  lasts  a  little 
longer,  and  may  even  persist  and  increase  in  distinctness  through 
the  short  pause  up  to  the  succeeding  second  sound.  It  is  so  common 
for  some  degree  of  obstruction  to  be  combined  with  regurgitation 


Yui.   40. — I'oiKT    OK    Maximum    ALUuiiLiTV 

(SIIADED)     AND     AkEA     OF      TbANSMISSIOX 

(outlined)     ok      Mitral     Rkoiuoitant 
Murmur. 


MITRAL   REGURGITATION 


243 


that  a  shorter  or  longer  presystolic  murmur  often  ushers  in  the 
systolic  bruit.  It  forms  but  an  added  element,  and  in  nowise 
alters  the  fact  stated  above — namely,  that  the  time  or  rhythm  of 
the  mitral  regurgitant  murmur  is  strictly  systolic  (Fig.  41). 


Fig.  41. — Time  of  Mitral  Keguegitant  Murmur. 
Red  shows  time  of  murmur.     Cardiac  cycle  as  in  Fig.  9.    Eead  from  left  to  right. 


The  next  element  of  importance  is  its  position  of  maximum 
intensity.  The  bruit  in  some  cases  is  heard  most  clearly  near  the 
anatomic  situation  of  the  mitral  valve — i.  e.,  at  the  level  of  the 
fourth  costal  cartilage  near  the  left  border  of  the  sternum,  but  as 
a  general  rule  the  murmur  is  conducted  along  the  chest-wall  to  the 
point  where  the  apex  of  the  heart  strikes  with  greatest  force. 
Hence  the  murmur  is  heard  most  loudly  in  the  immediate  vicinity 
of  the  apex-beat,  sometimes  slightly  within,  sometimes  just  above 
the  nipple,  and  sometimes  a  little  to  the  outer  side  of  the  apex. 
It  is,  however,  louder  in  this  than  in  any  other  cardiac  area,  and 
by  reason  of  this  circumstance  recognised  as  mitral. 

Very  rarely  a  mitral  regurgitant  bruit  is  heard  more  plainly 
in  the  tricuspid  area — i.  e.,  on  the  ensiform  appendix  or  close  to 
its  left  margin — when  it  is  likely  to  be  mistaken  for  a  tricuspid 
bruit.  I  have  known  such  a  mistake  to  be  made  in  more  than  one 
instance.  The  error  can  be  avoided  by  attention  to  the  signs  of 
tricuspid  regurgitation,  as  described  in  that  chapter. 

Inexperienced  auscultators  are  apt  to  attach  a  wrong  impor- 


244  DISEASES  OF   THE  HEART 

tance  to  the  intensity  and  the  quality  of  a  murmnr.  It  goes  with- 
out saying  that  all  possible  differences  in  these  respects  are  to  be 
found  in  mitral  systolic  murmurs  depending  upon  conditions  gov- 
erning their  generation.  Neither  the  loudness  nor  the  quality  of 
a  bruit  furnishes  any  evidence  per  se  as  to  the  gravity  of  the 
lesion.  A  very  intense  musical  murmur  may  be  produced  by  the 
blood-stream  being  forcibly  dri^•en  through  a  small  aperture,  and 
conversely  a  very  widely  open  and  unguarded  orifice  may  permit 
the  blood  to  regurgitate  so  easily  and  noiselessly  that  only  a  very 
soft,  scarcely  audible  inurmur  is  generated.  Hence  neither  inten- 
sity nor  quality  of  a  murmur  is  of  importance  in  determining 
whether  or  not  it  is  mitral;  they  only  facilitate  the  detection  of 
the  murmur,  and  sometimes  aid  us  in  determining  the  seriousness 
of  the  lesion. 

Furthermore,  the  intensity  of  the  murmur  is  governed  by 
other  circumstances  than  the  leak  itself.  The  bruit  of  mitral  re- 
gurgitation is  generally  loudest  during  energetic  action  of  the 
heart,  hence  during  excitement  and  immediately  after  exertion. 
It  is  consequently  brought  out  clearly  by  having  the  patient  jump 
about,  swing  the  arms  violently,  or  do  something  else  that  causes 
the  heart  to  beat  rapidly  and  energetically.  By  such  a  procedure 
it  is  often  possible  to  detect  a  mitral  bruit  which  before  was  in- 
audible or  so  indefinite  as  to  have  left  the  examiner  in  doubt  of  its 
existence. 

The  position  of  the  patient's  body  also  influences  the  audibil- 
ity of  the  murmur.  It  is  in  most  cases  heard  most  plainly  when 
the  patient  sits  or  stands,  but  I  have  frequently  seen  cases  in  which 
it  came  out  far  more  distinctly  in  the  dorsal  decubitus,  which  per- 
mitted the  heart  to  beat  more  forcibly  because  more  slowly.  Con- 
sequently, it  should  be  an  invariable  rule  to  auscultate  a  suspected 
case  of  mitral  insufficiency,  and  indeed  any  suspected  case  of  car- 
diac disease,  in  all  tliree  positions.  It  will  often  protect  one 
against  a  serious  blunder  in  diagnosis. 

Mitral  systolic  murmurs  are  usually  spoken  of  as  blowing  and 
soft.  They  are  as  a  matter  of  fact  softer  than  direct  murmurs  of 
stenosis,  but  they  are  by  no  means  always  soft.  They  may  be 
harsh  and  rasping,  or  filing,  grating,  sawing,  whistling,  etc.,  in 
which  event  they  are  designated  as  musical,  a  character  of  patho- 
logical but  scarcely  diagnostic  interest. 


MITRAL  REGURGITATION  245 

Finally,  mitral  systolic  iniirmurs  should  always  be  studied 
with  respect  to  the  direction  in  which  they  are  transmitted  from 
the  apex.  This  is  especially  important  in  cases  in  which  secondary 
physical  signs  of  mitral  regurgitation  are  difficult  to  obtain,  for  in 
such  cases  it  is  necessary  for  correct  diagnosis  to  determine 
whether  or  not  the  apex  systolic  bruit  is  an  accidental  one.  Such 
inorganic  murmurs  are  of  limited  propagation,  whereas  mitral 
regurgitant  bruits  are  often,  though  not  invariably,  Avidely  trans- 
mitted. Their  direction  of  propagation  is  towards  the  left  rather 
than  the  right,  and  therefore  they  may  be  traced  into  the  axillary 
region,  or,  as  sometimes  happens,  even  on  to  the  back.  It  is 
not  at  all  rare  to  hear  an  intense  mitral  murmur  at  the  inner 
side  of  the  left  scapula  near  its  tip,  and  in  children  such  a  bruit 
may  be  heard  throughout  the  entire  thorax.  When  in  any  case 
the  murmur  is  audible  in  more  than  one  area  it  is  indispensable 
to  determine  by  careful  comparison  in  which  area  it  is  of  maxi- 
mum intensity,  for  only  in  this  way  can  one  decide  to  what  car- 
diac area  the  murmur  belongs. 

One  is  not  to  content  himself  with  studying  only  the  murmur, 
he  must  also  carefully  auscultate  the  several  heart-sounds.  If  the 
first  tone  at  the  apex  is  not  replaced  by  the  murmur,  it  offers  a 
certain  amount  of  evidence  in  favour  of  the  valve  being  not  wholly 
destroyed,  but  able  to  still  partially  close  the  orifice.  If,  on  the 
other  hand,  the  murmur  alone  is  heard,  it  indicates  great  freedom 
of  regurgitation.  Then  one  should  note  the  degree  of  accentuation 
and  purity  of  the  pulmonic  second  sound,  especially  in  all  cases 
in  which  the  interpretation  of  the  murmur  is  not  clear.  Regurgi- 
tation by  inducing  pulmonary  congestion  leads  to  intensification 
of  the  pulmonic  second  tone,  and  hence  such  intensification  is  the 
earliest  recognisable  secondary  physical  sign  of  mitral  insuffi- 
ciency, and  greatly  strengthens  the  inference  drawn  from  the  rec- 
ognition of  a  murmur. 

Diagnosis. — The  diagnosis  of  mitral  regurgitation  is  not  diffi- 
cult as  a  rule,  being  in  some  instances  one  of  the  easiest  of  all 
valvular  lesions  to  make  out.  When,  however,  the  leak  is  slight, 
the  murmur  obscure,  and  the  secondary  changes  in  the  heart  and 
general  circulation  insignificant,  its  diagnosis  may  be  anything 
but  easy.  It  is  also  occasionally  difficult  when  there  is  dropsy,  a 
rapid,  tumultuous  action  of  the  heart,  extensive  dilatation,  and 


246  DISEASES  OF  THE  HEART 

serous  accunuilation  in  the  pleural  cavities.  One  may  then  make  a 
diagnosis  of  the  condition  with  reservation,  and  wait  for  treatment 
to  clear  up  the  case.  Attention  to  the  secondary  physical  signs 
will  usually  help  out  amazingly  under  such  circumstances. 

The  history  of  the  patient  is  also  of  great  importance,  not 
alone  to  the  diagnosis  of  mitral  insufficiency,  but  to  the  recognition 
of  the  etiology,  and  thereby  to  the  relative  or  organic  nature  of 
the  regurgitation.  Its  gravity  is  to  be  determined  by  the  second- 
ary effects  which  the  heart-walls  and  cavities  have  undergone, 
and  by  the  presence  or  absence  of  symptoms  referable  to  the  car- 
diac disease.  Not  until  all  this  has  been  accomplished  should  the 
physician  rest  satisfied,  remembering  that  the  detection  of  a  mur- 
mur does  not  constitute  a  diagnosis. 

Prognosis. — In  general,  it  may  be  stated  that  mitral  regur- 
gitation affords  a  more  favourable  prognosis  than  does  any  other 
valvular  disease,  yet  in  this  respect  each  case  is  a  law  unto  itself. 
Furthermore,  the  prognosis  of  each  case  depends  upon  many  dif- 
ferent factors:  (1)  On  the  etiological  nature  of  the  defect,  (2) 
its  severity,  (3)  the  degree  of  secondary  effects,  (4)  the  complete- 
ness of  compensation,  and  (5)  the  existence  or  not  of  complica- 
tions, such  as  other  valvular  lesions  and  adherent  pericardium. 

Insufficiency  of  the  mitral  valve  from  sclerosis  furnishes  as  a 
rule  less  favourable  prognosis  than  does  that  of  endocarditis, 
because  of  the  progressive  tendency  of  the  sclerotic  change  and  of 
the  age  of  the  patient,  which  renders  it  likely  that  the  myocardium 
is  no  longer  healthy.  If  the  regurgitation  is  free,  if  secondary 
hypertrophy  and  dilatation  are  extensive,  if  engorgement  of  the 
general  viscera  is  apparent,  even  though  compensation  seems  ade- 
quate, the  prospect  of  the  disease  remaining  stationary  is  not 
good.  If  mitral  regurgitation  is  united  with  defects  of  other 
valves  or  orifices,  the  prognosis  is  correspondingly  unfavourable. 
Complications  on  the  part  of  the  pericardium  and  of  chronic 
nephritis  render  prognosis  very  unfavourable.  Finally,  prognosis 
stands  in  direct  relation  to  the  completeness  of  the  compensation. 

The  curability  of  this  lesion  resulting  from  endocarditis  has 
been  much  discussed,  and,  as  pointed  out  by  Balfour  and  others, 
seems  certainly  possible.  This  is  considered  particularly  true 
after  chorea. 

The  influence  of  age,  sex,  occupation,  environment,  etc.,  will 


MITRAL  REGURGITATION  247 

be  considered  in  a  subsequent  chapter  devoted  to  the  Prognosis  of 
Valvular  Disease  in  General. 

Mode  and  Causes  of  Death. — A  patient  with  uncompli- 
cated mitral  incompetence  rarely  dies  suddenly  and  without  warn- 
ing, as  in  some  otlier  forms  of  heart-disease.  When,  however,  this 
lesion  is  united  with  fatty  or  fibroid  degeneration  of  the  heart- 
muscle  the  individual  may  drop  dead  from  sudden  diastolic  arrest. 
I  have  known  one  such  instance  in  a  man  of  sixty.  A  long  period 
of  suffering  may  be  terminated  by  a  rather  rapidly  developed 
pulmonary  oedema,  but  usually  the  end  comes  slowly  through  grad- 
ually increasing  cardiac  exhaustion  and  weeks  or  even  months  of 
most  distressing  symptoms. 

Very  rarely,  death  may  take  place  from  embolic  plugging  of 
the  pulmonary  artery  or  one  of  its  main  branches,  but  such  a 
sequence  is  usually  preceded  by  symptoms  of  cardiac  asthenia. 

In  one  instance  a  young  woman  died  suddenly  under  the  fol- 
lowing circumstances :  About  a  week  before  her  death  she  had 
sought  medical  advice  on  account  of  increasing  dyspnoea,  and  was 
found  to  present  signs  of  combined  mitral  incompetence  and  ob- 
struction due  to  articular  rheumatism  some  years  before.  Be- 
cause of  failing  compensation  she  was  ordered  to  rest  quietly  at 
home ;  notwithstanding  this,  she  a  few  days  later  carried  a  buck- 
etful of  coal  upstairs.  The  next  morning  her  speech  was  thick, 
she  complained  of  stiffness  in  the  back  of  the  neck,  and  showed  a 
degree  or  so  of  temperature,  but  evinced  no  paralysis.  She  was 
then  sent  to  the  hospital,  and  a  day  or  two  later,  upon  sitting  up 
in  bed  to  drink  a  cup  of  tea,  suddenly  fell  back  upon  the  pillow 
and  expired.     A  post-mortem  examination  could  not  be  obtained. 

Another  female  patient  who  for  eleven  years  had  evinced 
symptoms  and  physical  signs  of  a  double  mitral  lesion  with  adher- 
ent pericardium,  at  length  began  to  suffer  from  increasingly  fre- 
quent attacks  that  seemed  to  indicate  a  sudden  augmentation  of 
stasis  within  the  pulmonary  vessels,  yet  without  other  manifesta- 
tions of  more  than  usual  cardiac  weakness.  Serous  transudation 
could  nowhere  be  detected.  The  final  attack  lasted  but  a  few 
hours,  and  seemed  to  be  the  result  of  a  rapidly  increasing  failure 
on  the  part  of  the  right  ventricle.     'Eo  necropsy  was  permitted. 

A  lad  of  twelve  years  with  chronic  mitral  regurgitation  of 
rheumatic  origin  in  whom  a  badly  broken  compensation  had  been 


248  DISEASES  OP   THE   HEART 

partially  restored,  and  who  a  few  weeks  before  death  seemed  to 
have  contracted  a  fresh  inflammation  of  the  mitral  orifice,  arose 
from  bed  earlv  one  morning  to  pass  urine ;  he  had  scarcely  made 
the  attempt  when  he  fell  on  his  pillow  in  a  condition  that  alarmed 
his  nurse.  Two  hours  later  I  found  him  partly  unconscious,  and 
with  a  moderately  slow  and  irregular  pulse.  He  was  pronounced 
moribund,  and  death  occurred  an  hour  or  two  subsequently.  Un- 
fortunately, post-mortem  examination  could  not  be  obtained,  and 
as  in  the  two  preceding  cases,  the  immediate  cause  of  death  could 
only  be  conjectured.  It  was  probably  due  to  an  acute  overdisten- 
tion  of  the  heart,  leading  to  gradual  paralysis. 

Hustedt  examined  491  cases  of  heart-disease  at  the  Patho- 
logical Institute  at  Kiel,  with  a  view  to  determining  the  causes  of 
death.  Of  15  cases  of  mitral  insufficiency,  without  associated  car- 
diac lesionSj  he  found  the  following  causes  of  death:  Cardiac 
asthenia  (Herzschwiiche),  7  cases;  pulmonary  infarct,  2  cases; 
apoplexy  due  to  embolism,  1  case,  while  in  the  other  5  death  was 
due  to  some  accidental  or  intercurrent  affection,  such  as  nephritis 
1,  peritonitis  2,  marasmus  1,  pulmonary  collapse  1. 


CHAPTER    VII 
MITRAL   STENOSIS 

This  term  denotes  a  narrowing  or  constriction  of  the  opening 
between  the  left  auricle  and  ventricle,  in  consequence  of  which 
there  is  an  obstruction  to  the  free  flow  of  blood  from  the  former 
into  the  latter  chamber.  A  narrowing  is  always  the  result  of  struc- 
tural defect,  either  of  the  ring  itself,  of  the  valve,  or  of  both,  and 
can  never  be  of  a  functional  or  relative  kind,  analogous  to  relative 
incompetence  of  the  valves.  The  stenosis  may  be  congenital  in 
consequence  of  defect  of  development,  or  of  endocarditis  during 
intra-uterine  life,  but  in  the  great  majority  of  cases  it  is  acquired 
after  birth,  and  forms  one  of  the  most  frequently  encountered  of 
all  valvular  lesions. 

Morbid  Anatomy. — In  a  well-marked  case  of  mitral  steno- 
sis the  cusps  are  thickened  and  rigid,  they  are  adherent,  and  bound 
firmly  in  place  by  the  thickened  and  contracted  chordae  tendinese 
and  papillary  muscles.  The  whole  valvular  structure  is  thus  often 
converted  into  a  rigid  funnel-shaped  opening,  with  a  narrow  slit- 
like extremity  of  size  scarcely  to  admit  a  small  probe.  This  is  the 
so-called  buttonhole  mitral  (Fig.  42),  and  in  this  form  of  steno- 
sis the  endocardium  may  present  no  evidence  of  old  vegetations, 
but  be  perfectly  smooth.  This  has  led  some  French  authors  to 
consider  the  condition  one  of  congenital  malformation  rather  than 
of  rheumatic  origin.  Sansom,  on  the  other  hand,  thinks  it  due  to 
inflammation,  and  that  its  smoothness  results  from  the  "  quasi- 
cicatricial  tissue  "  being  subjected  to  pressure  by  the  blood  on 
both  its  auricular  and  ventricular  aspect. 

The  stenosed  valves  often  show,  however,  marked  evidence  of 
past  inflammation  in  the  form  of  organized  or  calcified  thrombi, 
especially  on  the  auricular  surface.  These  may  be  so  large  as  to 
almost  completely  obstruct  the  orifice,  while  their  presence  always 
leads  to  shrinkage  and  deformity  of  the  valve,  and  almost  always 
18  249 


250 


DISEASES  OF  THE   HEART 


to  a  certain  anioimt  of  regurgitation.     In  fact  a  pure  stenosis  is 
very  rare,  although  it  does  occasionally  occur. 

Campbell  ingeniously  suggests  that  the  shape  of  the  orifice  de- 


termines the  amount  of  the  discharge.  The  shape  of  an  orifice 
and  the  passage  leading  up  to  and  away  from  it  influence  the  quan- 
tity of  fluid  that  can  pass  through  it  in  a  given  time.     ''  If  a  round 


MITRAL  STENOSIS  251 

hole  be  pimctnred  in  a  can  full  of  water,  the  cross-section  of  the 
fluid  jet  coming  from  it  is  much  less  than  the  area  of  the  aper- 
ture, little  more  than  half  of  it.  The  relation  of  one  to  the  other 
is  termed  the  coefficient  of  discharge.  If  now  the  small  end  of  a 
funnel  be  accurately  fitted  to  the  inner  side  of  the  aperture,  so  as 
to  imitate  the  condition  of  things  obtaining  in  the  funnel  mitral, 
the  coelficient  of  discharge  is  almost  doubled.  Again,  if  instead  of 
making  a  round  aperture  in  our  can  we  make  a  linear  one,  so  as  to 
imitate  the  buttonhole  mitral,  we  in  a  similar  way  nearly  double 
the  coefficient  of  discharge.  This  form  of  the  mitral  orifice  results 
from  the  flattening  out  of  the  funnel  through  cicatricial  contrac- 
tion, so  as  to  form  a  more  or  less  flat  diaphragm,  and  it  is  indeed 
a  remarkable  fact  that  in  this  process  the  round  aperture  of  the 
funnel  is  invariably  converted  into  a  slit.  Sometimes  it  will  seem 
to  be  slit-shaped  before  the  flattening-out  process  begins.  Hence 
it  is  clear  that  in  mitral  obstruction  the  heart  avails  itself  in  a 
very  cunning  way  of  principles  well  known  to  the  engineer,  so  as 
to  secure  the  maximum  flow  through  the  narrowed  mitral  orifice — 
a  brave  attempt  to  make  the  best  of  a  bad  job." 

It  seems  possible,  however,  that  the  fact  of  the  mitral  valve 
being  composed  of  two  approximately  triangular  leaflets,  which 
become  adherent  along  their  sides,  and  leave  a  small  opening  at 
their  apices,  where  the  two  flat  cusps  come  together,  may  have 
something  to  do  with  the  slit-like  shape  of  the  stenosed  orifice. 

The  effect  of  narrowing  of  the  mitral  orifice  is  to  increase  the 
difficulty  with  which  the  left  auricle  expels  its  contents  into  the 
ventricle.  The  reaction  of  the  musculature  to  this  increased  de- 
mand for  work  is  shown  by  the  production  of  hypertrophy.  This 
is  the  primary  effect ;  and  dilatation,  when  it  does  occur,  is  a  later 
event.  In  mitral  incompetence,  on  the  other  hand,  dilatation 
comes  first  and  hypertrophy  afterward.  Yet  there  are  many  cases 
of  mitral  stenosis  in  which  the  auricle  is  found  post  mortem  to  be 
thin-walled  and  dilated.  This  is  probably  in  most  cases  due  to 
associated  regurgitation,  for  in  a  series  of  cases  taken  from  the 
records  of  Guy's  Hospital,  Samways  found  that  the  degree  of  dila- 
tation was  nearly  always  proportional  to  the  amount  of  leakage 
associated  with  the  stenosis. 

The  left  ventricle  presents  a  condition  in  marked  contrast  to 
that  found  in  regurgitation.     The  narrowed  orifice  allows  only  a 


252  DISEASES  OF  THE  HEART 

reduced  amount  of  blood  to  pass  into  the  ventricle  with  auricular 
systole,  and  hence  the  work  required  of  the  ventricle  is  reduced. 
The  chamber  becomes  diminished  in  size,  and  its  walls  thin  and 
weak.  At  times  this  atrophy  of  the  ventricle  is  so  marked  that 
the  chamber  is  almost  rudimentary  in  appearance. 

The  effects  of  mitral  stenosis  on  the  circulation,  pulmonic  and 
systemic,  are  practically  those  of  insufficiency,  being  primarily  due 
to  obstruction  of  the  blood  in  the  pulmonary  veins.  The  obstruc- 
tion is  more  constant  and  unyielding  in  stenosis,  however,  and 
hence  the  congestive  effect  is  even  more  marked  than  in  insuffi- 
ciency. 

The  effect  on  the  myocardium  in  producing  brown  atrophy, 
and  the  congestion  of  the  various  organs  of  the  body,  are  the  same 
as  in  mitral  incom})etenee,  and  do  not  call  for  repetition. 

Etiology. — Much  of  what  has  been  said  concerning  the  causa- 
tion of  mitral  regurgitation  applies  equally  to  narroM'ing  of  the 
mitral  ostium.  There  is  one  great  difference  between  the  two, 
however — namely,  stenosis  cannot  be  anything  else  than  a  struc- 
tural defect,  and  therefore  it  results  either  from  changes  during 
fcetal  existence  or  from  endocarditis  or  sclerotic  changes  after 
birth.  Acute  inflammation  usually  produces  clinical  phenomena 
of  incompetence  and  not  narrowing,  but  changes  initiated  during 
an  acute  attack  may  subsequently  develop  into  such  as  cause  pro- 
nounced obstruction. 

Mitral  stenosis  results  most  often,  therefore,  from  subacute  or 
chronic  rheumatism,  and  on  this  account  is  a  progressive  lesion. 
Accordingly,  as  pointed  out  by  Sansom,  it  is  especially  apt  to  be 
observed  in  persons  who  either  give  no  history  of  acute  rheumatic 
attacks  or  have  suffered  from  vague  joint  pains.  It  is  probable, 
therefore,  that  in  the  majority  of  cases  mitral  stenosis  is  of  rheu- 
matic origin,  but  of  the  insidious  or  masked  type,  and  not  of  the 
pronounced  form.  Nevertheless,  as  previousy  stated,  a  valvulitis 
initiated  during  an  attack  of  rheumatic  fever  may  in  time  even- 
tuate in  a  predominating  obstruction. 

Another  interesting  view  of  the  etiology  of  this  lesion,  and 
one  that  merits  consideration,  is  that  it  has  its  origin  in  tubercu- 
losis. This  opinion  was  announced  by  Teissier  as  a  result  of  his 
study  of  a  large  ninnbcr  of  cases.  Altliongli  j)ositive  evidence  of 
the  correctness  of  his  views  caimot  be  obtained,  as  he  himself 


MITRAL  STENOSIS  253 

admits,  he  yet  believes  that  tuberculosis  lies  at  the  bottom  of  the 
cases  of  mitral  stenosis  which  are  progressive. 

While  very  loath  to  accept  Teissier's  conclusions,  I  am  never- 
theless greatly  interested  in  the  possibility  of  such  a  causative 
relationship,  for  the  reason  that  prior  to  my  knowledge  of  his 
views  I  had  been  struck  with  the  fact  that  several  times  I  had 
encountered  narrowing  of  the  mitral  orifice  in  young  women  be- 
longing to  tuberculous  families.  I  recall  distinctly  a  young  Irish 
girl  who  had  lost  a  sister  from  consumption  and  sought  my  opinion 
and  treatment  because  she  feared  she  w^as  going  into  a  decline. 
The  character  of  the  respiratory  murmur  at  the  left  apex  made  me 
very  uneasy,  and  hesitate  about  expressing  an  opinion  until  after 
I  had  kept  her  under  observation  for  a  sufiicient  time  to  note  any 
changes  that  might  take  place  for  better  or  worse.  To  my  great 
surprise  I  at  length,  after  repeated  examinations,  discovered  signs 
that  indicated  a  very  slight  and  progressive  mitral  stenosis.  After 
the  lapse  of  a  number  of  months,  during  which  she  occasionally 
complained  of  vague  leg  pains  without  other  definite  indications 
of  rheumatism,  a  very  pretty  but  short  presystolic  murmur  became 
unmistakable. 

In  another  woman  of  twenty-nine,  wdio  also  had  lost  a  brother 
and  a  sister  of  consumption,  I  found  a  very  considerable  narrow- 
ing of  the  mitral  ostium,  as  evinced  by  the  secondary  signs  and 
symptoms  as  well  as  by  a  long,  rough,  loud  presystolic  bruit  and 
corresponding  thrill.  There  were  also  impaired  resonance  and 
broncho-vesicular  breathing  at  the  right  apex,  w^hich  made  me  very 
suspicious  of  latent  tuberculosis.  In  this  case  most  careful  and 
searching  inquiry  failed  to  elicit  a  history  of  previous  rheuma- 
tism or  leg  pains  in  childhood  that  might  have  been  construed 
as  rheumatic.  Nevertheless,  I  should  be  most  reluctant  to  say 
that  in  this  case  the  stenosis  was  of  tuberculous  origin.  To  my 
mind  it  is  far  more  reasonable  to  assume  that  she  had  had  unrec- 
ognised rheumatism.  Are  we  to  conclude  because  tubercle  bacilli 
have  been  identified  in  endocarditis  that  these  slowdy  progressive 
and  often  latent  cases  are  necessarily  of  tuberculous  causation  ? 
The  natural  delicacy  of  constitution  in  these  individuals  who 
come  of  tuberculous  stock,  and  the  frequency  with  which  rheuma- 
tism of  children  is  overlooked,  makes  far  more  plausible,  as  I 
take  it,  the  conclusion  that  the  valvular  defect  dates  from  early 


25i  DISEASES  OF  THE   HEART 

years  of  life,  and  has  taken  years  to  reach  that  degree  at  which  it 
becomes  clinically  recognised. 

Based  on  the  teaching  of  Rokitansky,  the  view  was  formerly 
held  that  there  is  a  natural  antagonism  between  narrowing  of  the 
mitral  ostium  and  pulmonary  tuberculosis  because  of  the  conges- 
tion of  the  lungs  produced  by  the  stenosis.  This  is  now  known  to 
be  erroneous,  for  pulmonary  tuberculosis  and  mitral  obstruction 
have  been  observed  conjointly  in  a  considerable  number  of  in- 
stances. Thus  Sansom  has  collected  31  cases  in  which  these  two 
diseases  were  found  associated  at  the  necropsy,  •  It  is  worthy  of 
note  also  that  of  these  31  cases  mitral  stenosis  and  tricuspid  steno- 
sis were  combined  in  11,  while  in  5  others  there  was  also  aortic 
valve-disease.  Sansom  explains  the  connection  of  pulmonary  con- 
sumption with  mitral  narrowing  on  the  ground  that  the  latter 
lessens  the  natural  resistance  of  the  organism  to  the  inroad  o£ 
tubercle  bacilli.  The  union  of  aortic  and  mitral  disease  intensifies 
this  susceptibility,  while  tricuspid  stenosis  predisposes  to  pulmo- 
nary tuberculosis  in  the  same  way  as  does  obstruction  at  the  pul- 
monic orifice. 

Syphilis  and  gout  are  etiological  factors  that  should  not  be  dis- 
regarded ;  but  they  lead  to  the  sclerotic  or  atheromatous,  not  to  the 
endocarditic  form  of  stenosis. 

The  influence  of  age  upon  the  type  of  the  disease  is  also  inter- 
esting. It  is  the  rheumatic  or  endocarditic  form  that  is  encoun- 
tered in  the  young.  This  is  shown  even  in  the  case  of  an  infant 
that  lived  l)ut  twenty-four  hours,  and  in  whom  Benezard  Smith 
discovered  mitral  stenosis  post  mortem,  and  likewise  in  the  infant 
of  four  months  observed  by  Gerhardt,  since  in  both  these  cases  the 
stenosis  was  evidently  the  result  of  endocarditis  during  foetal  life 
and  not  of  defective  development.  This  prevalence  of  mitral  ste- 
nosis in  the  young  (it  being  detected  most  frequently  at  or  about 
the  age  of  fourteen,  Sansom)  is  un(lonl)tedly  explicable  by  the 
fact  that  the  young  are  most  liable  to  articular  rheumatism.  On 
the  other  hand,  individuals  of  mi<ldle  age  or  over  develoj>  the 
sclerotic  form  of  this  valvular  lesion,  and  in  such  it  is  probably 
but  a  manifestation  of  a  general  tendency  to  fibrosis. 

The  association  of  mitral  stenosis  with  renal  disease  is  shown 
by  Goodhart's  statistics,  who  found  it  })resent  in  al)out  1.4  of  102 
cases  of  chronic  nephritis  that  came  tu  autopsy,  while  Pitt,  in  the 


MITKAL  STENOSIS  255 

post-mortem  records  of  Guy's  Hospital,  found  mitral  stenosis  and 
granular  kidney  three  times  as  frequently  as  stenosis  without  this 
form  of  renal  disease. 

It  is  a  striking  fact,  on  which  all  writers  comment,  that  mitral 
stenosis  is  encountered  far  more  frequently  in  the  female  than  in 
the  male  sex.  This  is  especially  true  of  the  disease  in  persons 
below  the  age  of  forty,  in  whom  it  is  probably  of  inflammatory 
origin,  while  the  sclerotic  form  of  the  lesion  does  not  appear  to 
predominate  greatly  in  either  sex.  Of  42  cases  of  pure  mitral 
stenosis  of  which  I  have  records,  28  occurred  in  females  and  14 
in  males,  and  of  the  entire  number  but  20  gave  a  clear  history  of 
rheumatism.  It  is  thus  seen  that  of  my  cases  females  numbered 
twice  as  many  as  males,  bearing  out  the  statement  that  mitral 
obstruction  is  par  excellence  a  disease  of  the  gentler  sex. 

Symptoms. — Inasmuch  as  the  effects  of  mitral  regurgitation 
and  mitral  stenosis  on  the  circulation  are  practically  the  same, 
there  is  a  close  similarity  in  the  symptoms  of  the  two  affections. 
Therefore,  much  of  what  was  said  under  the  head  of  mitral  regur- 
gitation also  applies  to  mitral  stenosis.  Undoubtedly  this  affec- 
tion may  remain  latent  for  years,  but  it  is  less  likely  to  do  so  than 
is  regurgitation.  Xevertheless,  hard  and  fast  lines  in  this  regard 
cannot  be  drawn,  for  the  manifest  reason  that  the  degree  of  the 
effect  stands  in  direct  proportion  to  the  gravity  of  the  lesion.  If 
compensation  is  adequate,  symptoms  referable  to  the  heart,  or  that 
call  the  attention  of  the  patient  to  his  heart,  may  be  entirely  ab- 
sent; and  yet  a  patient  with  any  considerable  degree  of  stenosis 
is  not  likely  to  be  robust,  or  to  possess  much  physical  endurance. 

Children  are  likely  to  be  more  or  less  stunted  in  development, 
both  mentally  and  bodily ;  while  in  the  case  of  adult  females  I 
have  been  impressed  by  the  frequency  with  which  they  are  tall  and 
thin,  with  evidence  of  anaemia.  Their  circulation,  as  might  be 
expected,  is  defective,  as  shown  by  coldness  of  the  hands  and  feet 
and  great  sensitiveness  to  low  temperature.  Even  when  not  suf- 
fering from  symptoms  referable  to  pulmonary  congestion,  as  dysp- 
noea, they  are  apt  to  complain  of  digestive  and  menstrual  disor- 
ders, sour  stomach  and  scanty  menstruation  being  particularly 
common.  They  are  generally  constipated  and  their  urine  is 
diminished  in  amount,  of  correspondingly  high  specific  gravity, 
and  loaded  with  urates. 


256  DISEASES   OF   THE   HEART 

Patients  with  mitral  stenosis  are  also  very  prone  to  attacks 
of  bronchitis,  -which  ultimately  run  into  chronic  bronchial  catarrh. 
They  are  also  particularly  liable  to  acute  pulmonary  oedema  upon 
extra  exertion,  and  in  such  instances  the  cough  and  haemoptysis 
or  frothy,  perhaps  blood-tinged,  sputum  often  give  rise  to  the  fear 
of  pulmonary  tuberculosis.  I  have  this  very  day  seen  a  well- 
marked  instance  of  the  kind. 

In  other  cases  there  is  persistent  dry  cough  due  to  bronchial 
congestion,  which  may  attract  attention  from  the  heart  to  the 
lungs.  I  well  remember  the  case  of  a  lady  who,  consulted  me  for 
an  obstinate  dry  cough,  which  was  found  due  to  a  mitral  stenosis, 
the  existence  of  which  had  not  been  suspected.  Indeed,  I  myself 
had  examined  her  about  a  year  previously  during  an  attack  of 
tachycardia,  and  at  that  time  was  unable  to  detect  any  implica- 
tion of  the  valves. 

As  a  rule  breathlessness  on  exertion  is  an  early  symptom  with 
patients  suffering  from  pronounced  mitral  constriction,  even 
though  in  all  other  respects  compensation  seems  good.  When  the 
narrowing  of  the  orifice  is  extreme,  when  the  heart-muscle  begins 
to  fail  from  degeneration  or  preponderating  dilatation,  dyspnoea 
becomes  an  exceedingly  distressing  symptom,  and  may  be  present, 
though  in  a  less  degree,  even  when  the  patient  is  at  rest.  Palpi- 
tations may  also  be  an  annoying  feature,  and  there  may  be  sharp 
or  dull  pnecordial  pains  with  areas  sensitive  to  pressure,  the  same 
as  in  mitral  regurgitation.  I  am  unable  to  recall  a  single  instance 
in  which  there  was  typical  angina  pectoris. 

In  other  cases  there  is  a  sense  of  pra'cordial  fulness  or  dis- 
tention, particularly  upon  exertion.  More  or  less  vertigo  declares 
itself  \\])im  the  patient  suddenly  assuming  the  erect  position,  or  he 
is  annoyed  by  a  feeling  of  fulness  or  confusion  in  the  head.  This, 
which  is  a  symptom  of  passive  cerebral  congestion,  often  amounts 
to  actual  headache.  Insomnia,  disturbing  dreams,  and  other 
effects  of  venous  congestion  become  more  and  more  pronounced, 
and  the  patient  passes  into  the  stage  of  completely  destroyed  com- 
pensation. 

Gi!dema,  which  is  at  first  confined  to  the  ankles  and  tends  to 
disappear  over  night,  creeps  upward  into  the  thighs,  rendering 
locomotion  difficult  and  painful.  Owing  to  the  feeble,  rapid,  and 
arrhythmic  action  of  the  overdistended  heart,  the  pulse  is  thready, 


MITRAL  STENOSIS  25T 

perhaps  unequal  in  the  two  wrists,  intermittent,  and  often  ex- 
tremely difficult  to  count.  This  intermittence  may  be  due  to 
cardiac  intermissions,  or  to  such  an  inequality  in  the  force  of  the 
heart's  contractions  that  some  of  the  blood-waves  fail  to  reach  the 
wrist.  The  hands  and  forearms  may  be  cold,  and  the  superficial 
veins  stand  out  prominently  in  striking  contrast  to  the  emptiness 
of  the  arteries. 

Pulmonary  congestion  declares  itself  by  increased  dyspnoea 
that  may  even  amount  to  orthopnoea,  by  cough  and  sero-mucous 
or  sero-sanguinolent  sputum,  dulness  at  the  bases  of  the  lungs,  par- 
ticularly behind,  and  by  copious,  moist  rales.  If  the  tricuspid 
valve  gives  way,  permitting  regurgitation  into  the  auricle,  the 
turgid  jugulars  pulsate.  The  liver,  already  swollen,  perhaps  ten- 
der, grows  still  more  engorged,  and  likewise  pulsates  synchro- 
nously with  the  epigastric  throbbing  of  the  dilated  right  ventricle 
and  the  so-called  positive  pulse  in  the  cervical  veins.  The  taking 
of  food  is  attended  with  formation  of  gas  that  distends  the  stom- 
ach and  bowels,  adding  greatly  to  the  patient's  distress,  and  ren- 
dering adequate  nourishment  difficult.  The  sufferer  frequently 
complains  of  dull  or  burning  pain  in  the  pit  of  the  stomach,  and  is 
tormented  by  an  intolerable  thirst.  Congestion  of  the  head  is 
shown  by  duskiness  of  the  countenance,  swimming  of  the  head, 
or  headache,  and  insomnia.  In  some  cases  there  is  a  condition  of 
somnolence,  and  the  sufferer  falls  into  short,  unrefreshing  naps, 
which  are  disturbed  by  dreams,  and  from  which  he  awakes  with  a 
start.  The  skin  is  not  infrequently  bedewed  by  a  cold  sweat, 
which  about  the  head  and  neck  may  be  so  copious  as  to  run  off  in 
trickling  streams. 

Stasis  within  the  renal  veins  leads  to  scantiness  of  the  urine, 
which  is  dark  in  colour,  loaded  with  urates,  and  often  contains 
albumin  and  casts.  The  action  of  the  bowel  becomes  irregular  and 
constipated,  or  as  the  dropsy  invades  the  abdominal  structures  the 
patient  may  be  annoyed  by  frequent  scanty,  liquid  stools.  Con- 
gestion of  the  hsemorrhoidal  veins  sometimes  gives  rise  to  addi- 
tional distress.  Disorders  of  the  pelvic  viscera  are  common  at 
this  time  in  the  female ;  the  catamenia  are  apt  to  be  scanty  and 
irregular,  and  leucorrho-a  is  not  uncommon.  Day  by  day  the  dis- 
tress of  the  patient  increases ;  during  his  waking  hours  he  longs  for 
the  relief  of  sleep  at  night,  and  by  night  his  discomfort  makes  him 


25S 


DISEASES   OF   THE   HEART 


long  in  turn  for  the  days.  Days  drag  on  into  weeks,  and  not  infre- 
quently weeks  into  months,  with  ever-augmenting  dropsy,  which 
at  length  invades  the  serous  cavities  (Fig.  43).  Ascites  and 
tumefaction    of    the    abdominal    walls    intensify   pressure    upon 

the  diaphragm  and 
abdominal  vessels, 
rendering  breath- 
ing still  more  la- 
boured. The  pres- 
sure thus  occa- 
sioned still  further 
impedes  the  re- 
turn flow  from  the 
veins  of  the  low- 
er extremities,  and 
causes  an  increase 
of  anasarca.  If 
hydrothorax  now 
sets  in,  the  pa- 
tient's shortness  of 
breath  becomes  ex- 
treme, and  he  is 
obliged  to  support 
his  body  by  resting 
his  arms  on  a  table 
in  front  of  him.     I 

Fig.  43. — Case  of  Mitkal  Stenosis,  showing  Ascites  and        i  i  r 

have  known  a  sut- 
ferer  from  mitral 
disease  in  this 
stage  to  remain  thus  for  several  weeks,  not  venturing  to  leave  her 
chair.  Fortunately  for  these  patients,  nature  is  not  able  long  to 
maintain  the  unequal  struggle,  and  unless  treatment  brings  relief, 
death  does  so  ere  long. 

Occasionally  in  this  extreme  stage  the  end  comes  through  sud- 
den stoppage  of  the  licart,  but  as  a  rule  it  is  the  result  of  some  one 
of  the  causes  that  will  be  narrated  in  the  part  of  this  subject  de- 
voted to  the  mode  of  death. 

Physical  Signs. — Inspection  is  apt  to  detect  more  or  less 
cyanosis,  and  in  pronounced  cases  there  may  be  distinct  blueness 


Clibbixg  of  Finger-tips. 
Areas  of  superficial  and  deep-seated  dulness  are  indicated. 


MITRAL  STENOSIS  259 

of  the  lips  and  finger-tips.  Patients,  particularly  children,  who 
have  had  the  disease  for  years  usually  display  clubbing  of  the 
terminal  phalanges.  Often  there  is  bulging  of  the  prsecordium, 
particularly  at  the  lower  end  of  the  sternum,  as  well  as  visible  epi- 
gastric pulsation.  If  compensatory  hypertrophy  is  great,  and 
lung-borders  are  retracted,  the  eye  may  discern  a  systolic  pulsation 
over  the  body  of  the  heart  and  a  short  diastolic  shock  in  the  pul- 
monary area  the  same  as  in  regurgitation.  The  apex-beat  is  usu- 
ally feeble,  and  not  likely  to  be  outside  of  the  nipple  or  below  its 
usual  situation. 

Palpation  confirms  the  impression  received  by  the  eye,  but  in 
addition  detects  a  thrill  at  the  apex,  which,  preceding  the  ventricu- 
lar impulse,  is  known  as  presystolic.  This  thrill  resembles  the 
purring  of  a  cat,  and  hence  is  called  "  fremissement  cataire."  It 
may  be  short  and  soft,  or  rough,  and  extend  throughout  the  greater 
part  of  diastole.  In  some  instances  a  shorter,  feebler  thrill  fol- 
lows the  second  sound,  occupying  the  forepart  of  the  diastolic 
period.  The  presystolic  thrill  is  found  to  lead  up  to,  and  termi- 
nate in  a  short,  sharp  systolic  shock  or  "  thumping  "  apex-beat. 
This  thrill  is  often  so  short  as  to  convey  the  impression  of  the 
apex-beat  being  split,  the  second  of  the  two  impulses  being  the 
sharper  and  stronger.  A  sharp  stroke,  imparted  by  the  sudden 
closure  of  the  pulmonic  valve,  is  sometimes  felt  distinctly  in  the 
second  left  interspace,  close  to  the  sternum.  Epigastric  pulsation 
is  generally  pronounced,  and  gives  the  impression  of  a  230werfully 
contracting  right  ventricle. 

In  compensated  cases  of  stenosis  the  pulse  is  small,  feeble,  and 
regular,  and  less  rapid  than  in  mitral  regurgitation. 

There  has  been  much  controversy,  chiefly  among  the  English, 
as  to  whether  the  pulse  of  mitral  obstruction  or  of  insufficiency  is 
the  more  likely  to  be  irregular.  This,  in  my  opinion,  is  a  matter 
of  slight  practical  importance,  and  yet  in  my  experience  I  have 
found  the  pulse  to  be  more  often  irregular  in  regurgitation  than  in 
stenosis. 

The  annexed  sphygmographic  tracing  (Fig.  44)  is  from  a  case 
of  pronounced  mitral  stenosis  in  a  female,  and  shows  the  pulse 
small,  of  high  tension,  and  regular.  When  pulse-tension  is  pro- 
nounced, it  is  due  to  capillary  resistance  and  not  to  the  energy  of 
left  ventricular  contraction.     Concerning  the  irregularity  of  the 


260 


DISEASES   OF   THE   HEART 


Fig.  44. — Sphygmogram  from  Case  of 

Mitral  Stenosis. 

(Personal  observation.) 


pulse  in  mitral  disease,  it  may  be  again  stated  that  observations  of 
Kadizewsky  appear  to  prove  that  the  character  of  the  pulse  in  this 
respect  depends  upon  the  state 
of  the  myocardium  of  the  au- 
ricles. When  this  is  healthy, 
the  pulse  is  regular ;  when 
degenerated,  either  fibroid  or 
fatty,  the  pulse  becomes  irreg- 
ular, even  arrhythmic. 

Popoff  has  called  attention  to  the  occasional  occurrence  of  a 
pulsus  differens  in  this  disease,  by  which  term  is  meant  an  ine- 
quality in  the  two  radial  pulses,  the  left  being  the  smaller.  As 
this  is  observed  when  compensation  is  destroyed,  and  may  dis- 
appear with  restoration  of  cardiac  energy,  Popoff  attributes  the 
inequality  to  pressure  of  the  greatly  dilated  left  auricle  on  the  left 
subclavian  artery.  Preble  has  also  noticed  its  occurrence  in  some 
of  his  cases.  As  pulsus  diiferens  may  also  be  produced  by  aneu- 
rysm, embolism,  thrombosis,  arteriosclerosis,  etc.,  it  is  important 

that  all  such  causes  be  ex- 
cluded before  the  phenomenon 
is  attributed  to  extreme  dila- 
tation of  the  auricle,  a  matter 
that  may  be  of  some  moment 
in  ]>rognosis. 

Percussion  shows  a  simi- 
lar change  in  absolute  and 
relative  cardiac  dulness  as  de- 
scribed in  the  article  on  mi- 
tral regurgitation — viz.,  an 
increase  of  cardiac  dulness 
towards  ilie  right  side  and 
downward  (Fig.  45).  This 
increase  bears  a  direct  rela- 
tion to  the  degree  of  stenosis. 
According  to  Leiibe,  percus- 
sion sliows  a  more  pronounced 
enlargement  of  the  right  heart  in  this  form  of  mitral  disease  than 
in  insufficiency,  a  point  he  regards  as  of  importance  in  the  differ- 
ential diagnosis  between  these  two  affections. 


Fig.  45. — Locaiion  ok  ApfcxiitAT  and 
Area  of  Deep-seated  Dulne.ss  in  Mi- 
tral Stenosis. 


MITRAL  STENOSIS 


261 


Another  difference  lies  in  the  fact  that,  owing  to  atrophy  in- 
stead of  hypertrophy  of  the  left  ventricle,  dulness  is  not  likely  to 
be  much  if  at  all  increased  to  the  left. 

Auscultation. — In  pronounced  cases  of  mitral  stenosis,  auscul- 
tation at  the  apex  of  the  heart  detects  a  murmur  of  such  intensity 
and  distinctive  character  that  it  at  once  fastens  the  attention  of 
the  examiner.  In  most  instances  it  is  a  long-drawn,  rough  bruit, 
which,  beginning  after  the  second  sound,  runs  up  to  and  termi- 


FiG.  46.- 


-Khythm  of  Chaeacteristic  Mukmue  of  Mitral  Stenosis, 
"  Auricular-Systolic." 


nates  abruptly  in  a  clear,  sharply  accented  first  sound.  The  mur- 
mur is  spoken  of,  therefore,  as  presystolic,  and  in  this  respect  cor- 
responds exactly  to  the  thrill  already  described.  When  well 
marked,  this  presystolic  murmur  is  so  striking  as  to  be  almost 
pathognomonic  of  mitral  obstruction  (Fig.  46). 

The  rhythm  of  this  bruit,  by  which  is  meant  the  time  of  its 
occurrence,  has  been  the  subject  of  considerable  controversy,  for 
the  reason  that  some  observers  have  declared  it  to  be  in  reality 
systolic  and  only  seemingly  presystolic.  The  generation  of  the 
first  sound,  say  they,  is  delayed  in  consequence  of  the  rigidity  of 
the  mitral  valve,  and  hence,  although  the  murmur  begins  with  the 
contraction  of  the  ventricle,  its  occurrence  prior  to  the  first  tone 
gives  it  the  appearance  of  preceding  ventricular  systole.  The 
arguments  in  support  of  this  opinion  have  never  convinced  me  of 


262 


DISEASES   OF   THE   HEART 


its  correctness,  and  consequently  I  regard  the  brnit  as  truly  pre- 
systolic. 

When  we  reflect  on  the  physiology  of  cardiac  action  we  see  that 
a  murmur  which  is  audible  before  ventricular  systole  is  generated 
during  diastole,  and  that  therefore  the  murmur  of  mitral  stenosis 
is  diastolic.  This  is  not  all,  however ;  the  bruit  in  most  cases  is 
plainly  heard  to  begin  in  the  latter  portion  of  the  long  pause — 
i.  e.,  the  diastolic  interval — and  to  end  exactly  with  the  first  tone. 
It  is  synchronous,  therefore,  with  the  contraction  of  the  left  auri- 
cle, which,  as  we  know,  takes  place  immediately  before  that  of  the 
ventricle.  For  the  reason,  then,  that  the  murmur  is  generated  dur- 
ing auricular  systole,  Gairdner  long  ago  proposed  the  name  for  it 
of  the  "  auricular  systolic  "  murmur. 

This  term  is  too  restricted,  however;  since,  as  is  well  known, 
the  bruit  in  some  cases  commences  before  the  contraction  of  the 

auricle,  in  fact  immediately 
after  the  second  sound,  and 
lasts  throughout  the  long 
pause.  It  is  consequently  a 
•liastolic  and  not  always  an 
auricular  systolic  murmur, 
and  as  such  is  in  contrast  to 
the  systolic  one  of  mitral  re- 
gurgitation. It  has  also  been 
c-alled  the  "  mitral  direct " 
murmur,  because  transmitted 
in  the  direction  of  the  blood- 
stream— i.  e.,  from  the  mitral 
opening  directly  to  the  apex 
of  the  left  venti"icle.  Indeed, 
it  may  be  stated  en  passant, 
that  all  bruits  of  stenosis  are 
called  direct  and  those  of  re- 
gurgitation indirect  iiniiimirs.  Considering,  then,  the  des-igna- 
tions  that  have  been  given  to  thf  murmur  in  question,  the  best  is 
the  one  in  most  general  use,  which  is  presystolic. 

The  murnuir  is  heard  most  distinctly  close  to  the  apex-beat, 
not  directly  at  the  seat  of  impulse,  but  slightly  within  and  above, 
at  the  point,  in  fact,  where  the  thrill  is  felt  most  plainly  (Fig. 


Fui.  47. — Akea  of  AruiHiLiTV  ok  tiik  I'he- 

SySTOLIC    MUKMUR    OF    MiTRAL    StENOSIS. 

It  is  frequently  limited  to  this  area. 


MITRAL  STENOSIS  263 

47).  Its  area  of  audibility  is  sometimes  very  limited,  being  con- 
fined to  the  immediate  proximity  of  the  apex,  but  I  have  known 
the  murmur  to  be  audible  for  a  considerable  distance  in  all  direc- 
tions, although  even  then  it  is  not  transmitted  so  widely  outside  of 
as  inside  of  and  above  the  apex-beat. 

The  quality  or  timbre  of  the  bruit  is  exceedingly  rough  and 
harsh,  so  that  it  is  frequently  described  as  rolling,  blubbering, 
spluttering,  etc.  Balfour  happily  describes  it  in  some  instances 
as  sounding  like  V-o-o-t  or  the  sound  produced  by  the  attempt  to 
roll  out  the  letters  R-r-b,  or  when  still  more  prolonged  R-r-r-b. 
The  final  consonant  of  these  combinations  is  supposed  to  represent 
the  short,  sharp  first  sound  that  terminates  the  bruit.  The  mur- 
mur never  possesses  the  soft,  blowing  quality  of  the  mitral  regur- 
gitant murmur,  since  obstructive  bruits  are  always  rougher  than 
those  of  regurgitation. 

The  length  and  intensity  of  a  presystolic  murmur  are  influ- 
enced by  posture  and  the  rate  of  cardiac  action.  Thus  a  bruit, 
which  is  short  and  rather  indistinct  when  the  heart  is  beating 
rapidly,  or  when  the  patient  is  standing,,  is  very  likely  to  increase 
appreciably  in  duration  and  to  display  its  true  character  more  dis- 
tinctly after  the  individual  has  lain  down  and  the  heart's  action 
has  become  slower.  In  other  instances  the  reverse  obtains,  the 
bruit  being  most  distinct  in  the  erect  posture.  One  should  aus- 
cultate in  all  positions  and  under  varying  conditions  of  cardiac 
action. 

Another  peculiarity  of  the  mitral  direct  murmur  is  its  change- 
ability, by  which  is  meant  that  it  is  not  always  the  same  in  dis- 
tinctness at  different  times.  I  recall  vividly  a  woman  in  whom  on 
several  occasions  I  felt  certain  of  the  existence  of  a  mitral  presys- 
tolic murmur.  On  one  occasion,  however,  after  an  absence  from 
observation  of  several  months,  her  heart  presented  no  such  mur- 
mur as  I  had  heard  before,  but  instead  a  feeble  first  sound  accom- 
panied by  a  faint  systolic  whiff.  Some  weeks  subsequently,  after 
having  taken  digitalis  and  strengthened  the  contractions  of  the 
left  auricle,  the  old-time  presystolic  murmur  reappeared.  Broad- 
bent  regards  this  changeability  as  of  great  significance  in  the  dif- 
ferential diagnosis  between  stenosis  and  regurgitation. 

The  foregoing  description  applies  to  most  cases  of  mitral  ob- 
struction, but  not  to  all,  and  as  it  is  the  exceptions  that  are  every 


26i 


DISEASES  OF   THE  HEART 


now  and  then  encountered,  they  will  now  be  described.  In  some 
instances  the  bruit  is  so  short  that  it  is  scarcely  recognisable  as 
separate  from  and  preceding  the  first  sound.  I  have  generally 
noted  in  such  cases,  however,  that  the  first  sound  is  short  and 
thumping,  and  appears  to  have  prefixed  to  it  a  short  thrill,  which 
causes  the  impulse  to  convey  to  the  hand  the  impression  of  its 
having  slidden  up  to  its  maximum  instead  of  having  given  a  clean 
thrust,  as  does  the  healthy  heart.  Difficult  as  it  is  to  recognise  this 
indistinct  or  abortive  murmur,  it  is  extremely  important  to  be  able 
to  do  so,  since  it  is  in  the  detection  of  obscure  signs  of  disease 
that  the  skilled  physician  differs  from  his  unskilled  colleague. 

The  reverse  of  this  short,  scarcely  recognisable  bruit  is  the 
long-drawn  murmur,  which  Traube  first  described  and  designated 
the  "  modified  presystolic  murmur."  This  is  the  murmur  which, 
commencing  directly  at  the  close  of  systole — i.  e.,  immediately 
after  the  second  sound — extends  through  the  long  pause  of  dias- 
tole, and  ends  with  the  next  first  sound  (Fig.  48).  A  not  at  all 
infrequent  auscultatory  finding  is  a  short  murmur  occurring 
after  the  second  sound  and  known  as  early  diastolic,  and  which  is 


Fio.  48. — Rhythm  of  Occasional  Variety  of  Mitual  Stenotic  Murmur,  thkouoh 
Entire  Ventrioixak  Diastole. 


tlien  succeeded  l)y  a  short  period  of  silence,  and  then  a  character- 
istic presystolic  murmur  (Fig.  49).  1'his  anomaly  is  therefore  a 
breaking  in  two,  as  it  were,  of  the  long  murmur,  and  by  Fraentzel 


MITRAL  STENOSIS 


265 


was  called  the  "  interrupted  modified  presystolic  murmur."  It  is 
very  diagnostic,  but  may  easily  mislead  an  inexperienced  auscul- 
tator.     Should  such  difficulty  of  interpretation  arise,  error  may  be 


Fig.  49. — "  Interrupted  Modified  Presystolic  "  Murmur  of  Mitral  Stenosis. 


avoided  by  due  attention  to  the  associated  secondary  physical  signs 
and  to  the  modifications  of  the  heart-sounds  soon  to  be  described. 

Another  departure  from  what  is  usually  heard  in  mitral  ste- 
nosis is  the  retention  of  the  presystolic  bruit  and  of  the  first  sound 
without  a  second  sound,  or  of  the  murmur  alone  ivithout  either  of 
the  cardiac  tones.  Attention  is  directed  to  these  anomalies  by 
Broadbent,  who  states  that  under  such  circumstances  it  is  possible 
for  the  murmur  to  be  mistaken  for  a  systolic  one  followed  by  a 
second  sound,  or  for  the  bruit  to  be  considered  systolic,  and  to 
have  replaced  the  sound  altogether.  Care  should  be  taken  to  avoid 
such  an  error,  since  a  systolic  murmur  means  regurgitation,  and 
for  sake  of  prognosis  as  well  as  treatment  stenosis  should  be  recog- 
nised as  such  whenever  it  exists.  A  mistake  can  probably  be 
avoided  by  palpation  of  the  carotid  pulse,  when  it  will  be  found 
that  this  is  preceded  by  the  murmur. 

Such  comparison  of  the  time  of  the  murmur  with  that  of  the 
carotid  pulse  is  likewise  valuable  when,  as  stated  by  Fraentzel,  the 
presystolic  murmur  disappears  in  the  last  weeks  of  life,  or  be- 
comes merged  into  a  systolic  one. 

The  various  modifications  in  rhythm  and  intensity  of  the 
19 


266  DISEASES  OF  THE  HEART 

mitral  obstructive  nmrnnir  are  due  to  differences  in  the  rapidity 
and  force  with  which  the  blood  flows  through  the  narrowed  orifice. 
It  is  conceivable — e.  g.,  that  during  the  fore  part  of  diastole  blood 
flows  too  gently  into  the  relaxed  ventricle  to  produce  sonorous 
eddies  and  vibrations.  When,  however,  it  is  energetically  pro- 
pelled by  auricular  contraction,  eddies  or  currents  are  generated 
of  sufiieient  force  to  give  rise  to  the  presystolic  murmur.  In  the 
same  manner  a  diastolic  murmur  following  the  second  tone  owes 
its  production  to  sonorous  eddies  generated  as  the  blood  gushes 
out  of  the  auricle  into  the  ventricle.  Then  as  blood-pressure  in 
the  ventricle  is  raised,  vibratory,  and  hence  audible  currents  cease 
for  a  time,  until  auricular  systole  again  throws  the  blood-stream 
into  sound-producing  currents  and  eddies.  Xarrowing  and  rough- 
ening of  the  mitral  orifice  furnish  all  the  conditions  essential  for 
the  generation  of  eddying  or  whirling  currents  in  the  blood-stream 
as  it  passes  the  ostium.  Yet  if  the  blood-flow  is  languid  the  eddies 
within  it  may  fail  to  set  up  vibrations  of  sufficient  force  to  be  con- 
ducted to  the  ear  or  hand  of  the  examiner.  This  explains  why 
shortly  before  death  or  during  times  of  great  cardiac  feebleness 
the  presystolic  murmur  may  disappear,  and  why  it  reappears  as 
heart-power  is  restored. 

Heart-sounds. — The  recognition  of  the  characteristic  murmur 
of  mitral  obstruction  is  not  enough ;  it  is  necessary  to  also  study 
and  recognise  peculiarities  in  the  heart-sounds.  In  well-marked 
cases  the  first  tone  at  the  apex  is  short  and  valvular,  or,  as  is  said, 
*'  thumping."  This  quality  is  so  peculiar  and  striking  as  to  be 
quite  distinctive  and  of  itself  sufficient  many  times  for  an  experi- 
enced auscultator  to  make  a  diagnosis  on  it  alone.  It  is  the  audi- 
tory impression  of  the  sharp,  quick  tap  that  forms  the  apex-beat 
in  this  disease. 

The  second  sound  at  the  apex  may  be  distinct,  but  in  most 
cases  it  is  indistinct.  At  the  base  of  the  heart  it  is  sometimes 
split  or  reduplicated  in  consequence  of  the  pulmonic  valve  being 
closed  a  fraction  of  a  second  later  than  the  aortic,  according  to  the 
law  tliat  the  valve  closure  is  delayed  in  that  artery  in  which  blood- 
pressure  is  the  higher.  In  ;(<1dition  also  the  ])uliii()nic  second  sound 
is  accentuated. 

The  phenomenon,  liowcvcr,  which  is  of  greatest  interest  in 
many  ways  is  what  is  tei-med  the  simulated  or  apparent  doubling 


MITRAL  STENOSIS  267 

of  the  second  sound.  This  is  to  be  distinguished  from  the  split- 
ting of  the  second  soimd  at  the  base.  It  is  limited  strictly  to  the 
mitral  area,  sometimes  to  the  very  site  of  the  apex-thrust,  and  con- 
sists in  the  occurrence  of  a  third  tone,  which  immediately  follows 
the  normal  second  sound.  English  clinicians  have  given  much 
study  to  this  apparent  doubling  of  the  second  sound,  and  have 
offered  a  variety  of  explanations  for  its  occurrence.  The  most 
reasonable  theory  is,  as  suggested  by  Sansom,  that  it  is.  in  some  way 
a  sound  of  valve-tension  being  produced  as  the  blood  gushes  forci- 
bly out  of  the  auricle  into  the  ventricle.  This  seems  borne  out  by 
the  observation  that  this  sound  sometimes  becomes  changed  into, 
or  replaced  by  an  early  diastolic  murmur.  Sansom  states  also  that 
this  double  sound  is  heard  at  some  time  or  other  in  all  cases  of 
mitral  stenosis,  and  indeed  may  in  some  instances  be  the  only  indi- 
cation of  the  lesion. 

When  this  auscultatory  phenomenon  is  present,  together  with 
a  presystolic  murmur,  it  forms  a  very  striking  assemblage  of 
sounds  that  cannot  possibly  be  mistaken  for  any  other  condition 
than  mitral  stenosis. 

I  have  known  this  doubling  of  the  second  sound  to  be  inappre- 
ciable when  the  heart  was  not  strong,  and  to  come  out  clearly  and 
beautifully  as  treatment  restored  cardiac  power.  When  the  heart 
beats  slowly  and  regularlj^  it  is  a  matter  of  no  difficulty  to  differ- 
entiate the  several  sounds  and  murmurs  heard  in  mitral  stenosis. 
When,  on  the  contrary,  the  rhythm  of  the  heart  is  disturbed,  the 
impression  may  be  received  of  an  indistinguishable  jumble  of 
sounds,  both  normal  and  adventitious.  Thus,  I  have  a  male  pa- 
tient with  a  rheumatic  mitral  narrowing  combined  with  a  slight 
degree  of  insufficiency  who  presents  such  a  jumble.  When,  as  now 
and  then  happens,  his  heart's  action  is  tolerabl}^  slow  and  regular 
I  hear  the  following:  A  rough  pres^'^stolic  murmur  ending  in  a 
thumping  first  sound,  then  an  exceedingly  brief  pause,  followed 
by  a  doubled,  or  apparently  doubled,  second  sound,  which  in  its 
turn  is  succeeded  by  a  short,  early  diastolic  murmur  and  a  short 
silence  preceding  the  next  presystolic  bruit.  At  times  a  short  sys- 
tolic murmur  accompanies  the  first  sound,  and  as  this  heart  is  gen- 
erally very  irregular  in  rhythm  it  can  better  be  imagined  than  de- 
scribed what  an  unintelligible  mixture  is  made  by  its  sounds  and 
murmurs. 


268  DISEASES  OF   THE  HEART 

Diagnosis. — The  diagnosis  of  mitral  stenosis  is  usually  a 
comparatively  sim2)le  matter.  It  may,  however,  be  difficult  and 
next  to  impossible  to  say  whether  it  or  insufficiency  is  present. 
Such  a  differentiation  is  important,  however,  from  the  standpoint 
of  prognosis  and  treatment,  and  should  be  made  when  possible. 
As  aids  in  this  direction  are  the  following:  (1)  Sex,  stenosis 
being  more  common  in  females,  regurgitation  in  males.  (2)  The 
short,  sharp  apex-beat  preceded  by  a  thrill  of  longer  or  shorter 
duration.  (3)  The  greater  extent  of  dulness  over  the  right  heart 
in  stenosis  with  stronger  and  more  distinct  epigastric  pulsation. 

(4)  A  rougher  lower  pitched  murmur  occurring  in  some  portion 
of  the  diastole,  usually  presystolic,  but  often  also  early  diastolic. 

(5)  Doubling  of  the  second  soimd,  limited  strictly  to  the  mitral 
area  or  to  the  apex.  (6)  The  likelihood  in  stenosis  of  more  pro- 
nounced secondary  effects  in  other  organs  than  the  heart.  (7) 
The  greater  smallness  and  feebleness  of  the  pulse  in  stenosis,  and 
the  greater  likelihood  of  arrhythmia  in  regurgitation. 

As  a  matter  of  fact  differential  diagnosis  is  not  likely  to  be 
difficult  except  in  the  stage  of  lost  compensation,  and  then  less  de- 
pendence must  be  placed  on  the  auscultatory  findings  than  on  the 
evidences  of  greater  secondary  effects  in  stenosis. 

In  all  cases  the  question  of  ascertaining  the  exact  nature  of  the 
lesion  is  not  all  of  diagnosis.  One  has  also,  or  in  addition,  to 
decide  the  degree  of  the  lesion  and  the  severity  of  its  effects,  and 
whether  or  not  the  findings  account  for  the  symptoms  complained 
of.  The  degree  must  be  determined  by  careful  consideration  of 
the  murmurs,  sounds,  and  secondary  effects.  The  longer  the  pre- 
systolic murmur,  the  more  thumping  the  first  sound  and  apex-beat, 
the  greater  the  enlargement  of  the  right  and  the  smaller  the  left 
ventricle,  the  feebler  and  smaller  the  pulse,  the  more  pronounced 
the  evidences  of  secondary  effects  on  the  liver — then  the  more  pro- 
nounced will  be  the  degree  of  narrowing.  The  association  of  a 
mitral  regurgitant  bruit  points  to  a  medium  degree  of  stenosis, 
and  so,  according  to  Sansom,  does  the  simulated  doubling  of  the 
second  sound  at  the  apex. 

Dyspna-a  on  even  sliglit  exertion,  as  slow  walking,  great  prone- 
ness  to  cough,  and  other  signs  of  bronchial  congestion,  a  feeling  of 
weakness  and  fatigue  out  of  proportion  to  the  effort  occasioning  it, 
scantiness  of  urine,  (■iii])tiii<'ss  of  the  arterial  system — are  all  symp- 


MITRAL  STENOSIS  269 

toms  indicative  of  serious  circulatory  embarrassment,  and  attribu- 
table to  the  valvular  disease. 

On  the  other  hand,  neuralgic  pains  in  the  pra^cordia  and  a 
feeling  of  fulness  or  uneasiness  in  the  cardiac  region,  coldness  and 
numbness  of  one  hand  and  not  the  other,  or  of  the  hands  and  not 
the  feet,  headache,  and  prolonged  vertigo,  the  patient  being  quiet 
and  the  pulse  not  feebler  than  usual,  a  feeling  of  nervousness  and 
restlessness — may  all  be  neurotic  manifestations  depending  on  de- 
fective nutrition  or  elimination,  and  in  such  cases  are  apt  to  be 
out  of  proportion  to  the  degree  of  the  lesion  and  to  symptoms  dis- 
tinctive of  cardiac  disease. 

Prognosis. — In  general,  this  is  less  favourable  than  that  of 
mitral  incompetence,  and  for  two  reasons:  (1)  Obstruction  is  con- 
stant and  tends  to  greater  stasis  in  the  pulmonic  vessels,  in  conse- 
quence of  which  the  left  auricle  and  right  ventricle  are  subjected 
to  greater  strain.  They  are  likely,  therefore,  to  break  in  their  com- 
pensation at  an  earlier  period.  (2)  Mitral  stenosis  is  a  progress- 
ive lesion,  and  may  under  the  influence  of  repeated  attacks  of  sub- 
acute rheumatism  become  at  length  so  extreme  that  life  cannot  be 
maintained. 

When  the  narrowing  is  pronounced  there  is  but  a  small  vol- 
ume of  blood  ejected  into  the  arterial  system,  general  nutrition  is 
correspondingly  poor,  complications  on  the  part  of  the  lungs  are 
more  likely,  outdoor  exercise  is  difficult  if  not  impossible,  normal 
metabolic  processes  are  interfered  with,  and  general  nutrition 
becomes  very  defective. 

In  a  word,  even  when  uncomplicated  and  apparently  well  com- 
pensated, mitral  stenosis  offers  an  exceedingly  grave  prognosis. 
By  some  authorities  the  average  length  of  life  is  set  down  as  not 
far  from  ten  years.  It  stands  next  to  aortic  regurgitation  in 
point  of  gravity. 

The  following  figures  are  of  interest  as  showing  the  average 
age  at  which  death  took  place  in  several  series  of  cases.  Of  San- 
som's  61  cases  death  occurred  at  32.7  years.  In  Hayden's  42  cases 
death  took  place  at  37.8  years.  Of  Broadbent's  53  cases  it  oc- 
curred at  33  years  for  males,  and  37  to  38  for  females.  Samways 
found  that  at  Guy's  Hospital  during  a  period  of  ten  years  the 
average  length  of  life  for  both  sexes  was  38.33  years;  in  less  pro- 
nounced forms,  43.6  years;  more  extreme  cases,  33.6  years. 


270  DISEASES   OF   THE   HEART 

The  influence  of  age,  habits,  occuijations,  environment,  etc., 
will  be  considered  in  the  chn]iter  devoted  to  Prognosis  in  General. 

Mode  and  Causes  of  Death.. — Death  in  eases  of  mitral 
stenosis  results  most  commonly  from  increase  of  cardiac  asthenia, 
the  same  as  in  mitral  regurgitation,  or  from  the  overpowering 
effects  on  the  heart  and  lungs  of  hydrothorax  and  stasis  in  the  pul- 
monary system.  Pulmonary  infarcts  are  particularly  liable  to 
occur,  and  nre  then  the  immediate  cause  of  death.  Sudden  death 
is  possible,  but  is  not  likely  except  in  the  terminal  stage^  when 
sudden  exertion  may  bring  about  diastolic  arrest  of  the  already 
overburdeued  heart. 

Even  when  compensation  is  fairly  good  the  patient  may  at  any 
time  succumb  to  an  attack  of  acute  bronchitis  or  pneumonia.  A 
lad  of  sixteen,  whose  compensation  allowed  him  to  occasionally 
enjoy  a  hunting  trip,  contracted  a  cold  on  such  a  trip,  and  died 
two  days  thereafter  of  what  was  thought  by  his  physician  to  be 
extreme  pulmonary  congestion.  An  attack  of  acute  pulmonary 
oedema  is  also  a  possible  cause  of  death  the  same  as  in  mitral  re- 
gurgitation. In  one  case  coming  under  my  knowledge  obstinate 
vomiting  contributed  largely  to  the  fatal  result  by  preventing 
retention  of  food  and  remedies.  The  end  appeared  to  come  as 
much  through  general  as  cardiac  exhaustion.  Death  may  be 
preceded  by  mild  delirium,  or  consciousness  may  be  retained 
to  the  last. 

Of  24  cases  analyzed  by  Hustedt  with  reference  to  causes  of 
death,  he  found  heart-weakness  in  8  cases,  pulmonary  infarct  in  1, 
pneumonia  in  4,  pulmonary  collapse  in  1,  emphysema  in  2,  apo- 
plexy in  .3,  bronchitis  in  1,  pleurisy  in  1,  meningitis  in  1,  perito- 
nitis in  1,  and  delirium  in  1. 

The  following  cases  illustrate  so  well  many  of  the  features  that 
have  been  dwelt  on  in  the  foregoing  pages  that  they  are  here 
appended : 

^Nfrs.  (A,  Irish-American,  aged  thirty-four,  was  admitted  to 
St.  Anthony's  Hospital,  November  20,  1900,  com])laining  of  breath- 
lessness  on  exertion,  cough,  and  frothy  white  sputum.  IJoth  par- 
ents had  died  of  heart-disease,  but  three  sisters  and  one  brother  were 
living  and  healthy.  The  patient  had  had  measles  and  pertussis  in 
childhood,  l)ut  no  rheumatism.  She  had  been  married  thirteen 
years,  had  six  children,  of  which  the  youngest  was  three,  and  had 


MITRAL  STENOSIS 


271 


had  six  abortions,  all  of  which  she  had  herself  induced,  and  which 
had  not  been  followed  by  chill  or  fever.  During  the  first  pregnancy 
she  had  had  cedema  of  the  left  leg,  passed  no  urine  for  two  days, 
and  had  come  near  ''  smothering,"  Her  physician  declared  she 
had  "  water  around  her  heart,"  and  had  tapped  her,  but  she  could 
not  say  whether  water  had  been  obtained  or  not.  She  had  been 
troubled  with  dyspna?a  on  exertion  for  a  number  of  years,  and  this 
had  always  been  particularly  bad  during  her  pregnancies! 

Examination  showed  a  woman  of  medium  height,  weighing 
114  pounds,  slight  cyanosis  about  lips,  cold,  moist  extremities,  and 
pulsation  of  the  external  jugu- 
lars, tongue  having  a  whitish 
coat  and  indented  by  the  teeth. 
The  pulse  was  134,  compres- 
sible, and  irregular  in  force 
and  volume,  but  there  was  no 
pitting  of  the  skin  over  the 
ankles  or  elsewhere.  The 
apex-beat  was  in  the  sixth  in- 
terspace, 4^  inches  to  left  of 
the  midsternal  line,  of  the 
character  of  a  faint  tap  in  an 
area  of  diffused  impulse  (Fig. 
50).  A  presystolic  thrill  ran 
up  to  and  ended  with  this 
faint,  sharp  tap,  and  there 
was  marked  epigastric  pulsa- 
tion. Relative  dulness  was  in- 
creased in  all  diameters,  from  third  interspace  to  sixth,  and  from 
2  inches  to  right  of  median  line  to  5  inches  to  left  of  the  same. 
The  first  sound  was  thumping,  heard  throughout  prtecordia,  and 
followed  quickly  by  a  scarcely  perceptible  second  sound,  the  aortic 
second  being  weak  and  the  pulmonic  second  markedly  accentuated. 
A  harsh  murmur  of  greatest  intensity  in  the  mitral  area  began  im- 
mediately after  the  second,  ran  up  to  and  ended  with  the  next 
ensuing  first  sound,  and  was  not  transmitted  into  the  axillary  re- 
gion. The  lungs  revealed  impaired  resonance  at  the  posterior 
bases,  with  some  moist  rales.  The  liver  was  palpable  two  finger- 
breadths  below  the  inferior  costal  margin,  but  the  spleen  was  not 


Fig.  50. — Location  of  Apex  and  Eelative 
Dulness  in  Case  of  Mitral  Stenosis 
(p.  270). 


272  DISEASES   OF   THE   HEART 

palpable,  and  there  was  no  evidence  of  free  fluid  in  the  abdomen. 
The  urine  was  scanty,  dark-coloured,  and  contained  a  trace  of  albu- 
min. The  temperature  was  98.6°  F.  and  respirations  28.  Her 
stomach  was  very  irritable,  and  for  several  days  she  had  not  been 
able  to  retain  nourishment. 

Four  hours  after  her  admission  her  pulse  had  increased  in 
rapidity  and  feebleness,  and  so  few  of  the  pulse-waves  reached  the 
wrist  that  the  heart-rate  had  to  be  counted  with  the  stethoscope.  It 
was  beating  180  per  minute.  Cyanosis  had  deepened,  cough  and 
dyspnoea  were  very  bad,  rales  had  grown  more  numerous,  and  the 
liver  had  increased  in  size.  Her  condition  was  so  critical  that  she 
was  given  a  hypodermic  injection  of  -|  of  a  grain  of  morphine  with 
■gi^  of  atropine,  nitroglycerin  y^^,  and  -gJ^  of  sulphate  of  strych- 
nine, this  latter  to  be  repeated  every  two  hours  during  the  night. 
An  ounce  of  sulphate  of  magnesia  was  also  administered,  and  a 
few  hours  subsequently  she  was  put  upon  10-minini  doses  of  tinc- 
ture of  digitalis  every  four  hours.  By  the  next  day  her  condition 
had  improved  materially,  the  pulse  coming  down  to  134,  and  being 
rather  more  regular,  but  the  strychnine,  digitalis,  and  a  daily  dose 
of  salts  were  continued.  Without  detailing  all  the  fluctuations 
of  this  patient  for  the  ensuing  ten  days,  it  may  be  said  that  the 
pulse  showed  ever-recurring  vagaries,  being  at  one  time  fairly 
regular,  all  waves  reaching  the  wrist,  and  at  others  being  rapid, 
irregular,  and  intermittent.  The  liver  also  varied  in  size,  dimin- 
ishing and  increasing  according  to  the  persistence  and  regularity 
with  which  the  salts  were  administered.  The  cough,  however, 
gradually  grew  less,  expectoration  diminished,  pain  left  the  epi- 
gastrium, she  retained  nourishment,  and  as  a  rule  got  several 
hours'  good  sleep  each  night.  As  the  condition  improved,  the 
strychnine  was  lessened  in  frequency  of  administration,  but  the 
digitalis  was  continued.  At  one  time  indeed  its  action  was  sup- 
plemented by  strophanthus.  At  length,  by  November  30th,  her 
pulse-rate  averaged  84,  and  it  was  recorded  that  all  the  waves 
reached  the  wrist.  Dulness  and  rfdes  had  left  the  lungs,  but  the 
liver  still  remained  palpable,  although  smaller  in  size.  The  pa- 
tient then  left  the  hos])ital  abruptly.  Two  months  subsequently 
she  again  re-entered,  complaining  as  before  of  cough  and  expec- 
toration, but  showing  no  dropsy.  Treatment  again  benefited  her, 
and  she  again  withdrew  from  observation.     I  am  indebted  for 


MITRAL  STENOSIS 


273 


the  notes  of  this  case  to  Dr.  J,  R.  Yung,  one  of  the  internes  at 
the  time. 

This  case  illustrates  fairly  well  the  symptoms  and  amenabil- 
ity to  treatment  of  a  case  of  mitral  stenosis  in  which  compensa- 
tion was  broken,  but  not  irreparably  so,  and  in  which,  with  signs 
of  stasis  amounting  even  to  a  relative  incompetence  of  the  tricus- 
pid valve,  there  was  no  oedema.  In  fact,  the  brunt  of  the  dis- 
turbance was  borne  mainly  by  the  lungs,  the  dulness  and  rales, 
the  dyspnoea,  cough,  and  frothy  expectoration  being  the  result  of 
the  great  pulmonary  engorgement.  It  is  hard  to  explain  why  in 
such  a  case  oedema  is  absent,  whereas  in  other  individuals  with 
apparently  no  greater  stasis,  dropsy  will  be  a  marked  and  dis- 
tressing feature.  It  certainly  seems  to  corroborate  the  view  that 
dropsy  depends  upon  the  state  of  the  blood  and  nutrition  of  the 
capillaries,  as  well  as  upon  the  degree  of  capillary  and  venous 
engorgement.  This  patient  subsequently  succumbed  to  a  third 
attack  in  the  hospital. 

Mr.  B.,  aged  twenty-nine,  tailor,  consulted  me  January  9, 
1900,  on  account  of  great  breathlessness  upon  the  slightest  effort. 
He  gave  a  history  of  rheuma- 
tism four  years  previous,  since 
which  time  he  had  suffered 
with  subacute  articular  pains. 
Gonorrhoea  six  years  ago, 
with  stricture  at  present  time. 
With  the  exception  of  a  ^^  bad 
eye,"  nature  unknown,  at  six 
years  of  age,  has  had  no  other 
illness.  Heart  began  to  trou- 
ble him  one  year  after  the 
rheumatic  attack,  but  was  not 
treated  for  heart-disease  until 
the  summer  of  1899.  His 
symptoms  were  great  dys- 
pnoea on  effort,  cough  once  in  a 
while  at  morning  and  evening, 
vertigo  upon  exercise,  some 
pain  between  the  shoulders,  and  poor  appetite,  but  sleep  good. 
His  pulse  while  sitting  was  weak,  small,  regular,  and  90.     The 


Fig.  51. — Location  uf  Ai'Ex  axu  Relative 
DuLNzss  IN  Case  of  Mitral  Stenosis 
AND  Kegdrgitation  (p.  273). 


274  DISEASES  OF  THE   HEART 

examination  of  the  heart  discovered  the  weak  apex-beat  at  the 
fifth  interspace,  nipple-line,  Sf  inches  from  median  line,  and 
preceded  by  a  short  thrill  (Fig.  51).  The  apex-beat  was  not 
thumping,  but  there  was  marked  epigastric  pulsation.  Abso- 
lute dulness  was  increased  from  right  border  of  sternum,  at  fourth 
costal  cartilage,  to  left  of  parasternal  line.  Relative  dulness 
from  lower  border  of  third  costal  cartilage  above  to  junction  of 
sixth  and  seventh  costal  cartilages  below,  If  inch  to  right  of 
median  line  and  to  f  of  an  inch  outside  of  nipple.  The  pulmonic 
second  sound  was  found  accentuated.  Second  sound  was  not 
doubled  at  base,  but  limited  to  area  of  the  apex-beat  was  an 
apparent  doubling  of  the  second  sound,  the  second  element  at 
times  having  the  character  of  a  short  murmur,  and  separated  from 
the  following  presystolic  murmur.  At  lower  inner  edge  of  the 
apex-beat  the  first  sound  was  also  doubled  at  times. 

A  short,  rough  presystolic  murmur  was  found  just  within, 
and  a  blowing  systolic  at  the  apex.  The  murmurs  and  sounds 
made  a  rolling,  tumbling  rhythm.  In  dorsal  decubitus  the  appar- 
ent doubling  of  second  sound  was  very  marked  at  inner  edge  of 
apex.  As  the  heart  occasionally  slowed,  the  first  sound  was  found 
also  doubled,  the  first  element  replacing  the  presystolic  murmur. 
The  systolic  murmur  became  plain  and  whistling  with  a  very  pro- 
nounced blow  2  inches  to  left  of  nipple.  The  liver  was  palpable 
a  finger-breadth  below  the  costal  arch. 

The  diagnosis  made  was  mitral  stenosis  and  insufficiency,  with 
secondary  cardiac  hyj)ertrophy  and  dilatation. 

Mrs.  A.,  aged  thirty-three  years,  weight  115  pounds,  height 
medium,  American,  was  examined  March  29,  1901.  Her  father 
was  living,  but  had  cough,  while  a  maternal  uncle  and  a  maternal 
aunt  had  died  of  consumption.  At  eighteen  she  had  suffered  from 
a  severe  attack  of  inflammatory  rheumatism,  and  had  had  more 
or  less  joint  pains  for  three  or  four  years  subsequently.  Of  chil- 
dren's diseases,  she  had  had  a  mild  attack  of  scarlatina  when  a 
child,  and  thought  that  during  her  childhood  she  had  also  had 
pleurisy.  She  had  had  a  .second  pleuritis  a  year  prior  to  her 
examination  by  me.  Her  present  illness  dated  back  to  1891, 
when  she  first  began  to  have  a  cough,  but  her  symptoms  had 
grown  much  worse  for  the  last  year,  and  she  had  grown  percep- 
tibly paler.     In  the  way  of  symptoms,  she  complained  chiefly  of 


MITRAL  STENOSIS  275 

chronic  cough,  which  was  most  troublesome  at  night,  and  of  con- 
siderable yellowish  sputum,  in  which  tubercle  bacilli  were  said  to 
have  been  discovered.  She  noticed  shortness  of  breath  in  walk- 
ing and  ascending  stairs.  The  appetite  was  poor  and  the  diges- 
tion weak,  although  bowel  movements  were  regular,  as  also  were 
the  menses.  Sleep  was  disturbed  by  the  cough,  and  there  was 
slight  pain  in  the  right  hip  and  the  left  side  of  the  chest  near  the 
shoulder.  The  voice  was  husky,  but  it  may  be  said  in  passing 
that  laryngoscopic  inspection  revealed  no  infiltration  of  the 
larynx. 

Examination. — The  pulse  was  105,  small,  regular,  and  of  no- 
ticeably low  tension.  The  temperature  taken  at  12  m.  was  99°  F. 
Respirations  were  shallow,  but  not  hurried.  The  chest  was  mod- 
erately emaciated,  very  shallow  in  its  antero-posterior  diameter, 
and  flattened  both  above  and  below  the  right  clavicle.  Vocal  frem- 
itus was  increased  at  both  apices,  particularly  the  right.  Upon 
the  right  side,  dulness  extended  from  the  apex  to  the  third  inter- 
space in  front  and  to  the  middle  of  the  scapula  behind,  shading 
off  to  impaired  resonance  as  far  as  the  tip  of  the  scapula  and 
below  this  point,  becoming  again  more  pronounced  towards  the 
posterior  axillary  line.  In  the  right  infraclavicular  region  there 
were  bronchial  breath-sounds,  moist  rales  of  varying  size,  and 
the  voice-sounds  were  so  concentrated  and  hollow  as  to  strongly 
suggest  a  cavity.  Posteriorly,  respiratory  sounds  were  also  bron- 
chial, and  the  act  of  coughing  developed  numerous  fine  and  coarse 
crackling  rales  as  far  down  as  the  inferior  scapula  angle.  At  the 
left  apex  there  was  impaired  resonance  both  front  and  back  to 
the  level  of  the  second  rib,  and  over  this  area  breath-sounds  were 
broncho-vesicular,  and  cough  produced  crumpling  rales  that  ex- 
tended below  the  limits  of  slight  dulness. 

The  apex-beat  was  situated  in  the  fifth  left  interspace  slightly 
within  the  liipple-line,  was  feeble,  and  of  the  character  of  a  quick 
thump,  and  was  preceded  by  a  short  yet  distinct  thrill  that  ended 
with  the  cardiac  impulse.  Relative  heart's  dulness  was  somewhat 
increased  towards  the  right  and  downward,  but  did  not  reach 
beyond  the  vertical  nipple-line  at  the  left  (Fig.  52).  Upon  aus- 
cultation the  first  sound  at  the  apex  was  short,  sharp,  and  thump- 
ing, the  second  sound  was  not  doubled,  and  the  pulmonic  second 
tone  was  markedly  accentuated.     A  rather  short,  rough,  distinctly 


276 


DISEASES  OF  THE  HEART 


presystolic  murmnr  ran  up  to  and  ended  abruptly  with  the  sharp 
first  sound,  and  was  of  greatest  intensity  in  the  standing  position. 

A  high-pitched  systolic  whiff 
accompanied  the  systole  in  the 
mitral  area,  but  was  not  trans- 
mitted to  any  appreciable  dis- 
tance outside  this  area. 

The  abdomen  was  flat  and 
thin,  the  lower  hepatic  border 
distinctly  palpable  and  tender 
to  pressure,  and  hepatic  dul- 
ness  reached  from  the  upper 
margin  of  the  sixth  rib  in  the 
mamillary  line  to  slightly  be- 
low the  inferior  costal  arch. 

The  diagnosis  was  clearly 
chronic  pulmonary  tuberculo- 
sis with  softening  and  vomica 
in  the  right  lung,  incipient 
disease  of  the  left  upper  lobe, 
mitral  stenosis  of  first  degree,  with  probably  some  regurgitation, 
the  valvular  lesion  being  of  rheumatic  origin  and  in  good  com- 
pensation. 

This  case  is  interesting  because  of  the  rather  rare  association 
of  pulmonary  tuberculosis  and  mitral  stenosis,  and  would  seem  to 
corroborate  the  view  that  this  valvular  lesion  is  sometimes  of 
tuberculous  origin,  were  it  not  for  the  very  definite  history  of 
inflammatory  rheumatism  at  the  age  of  eighteen.  It  likewise 
shows  the  fallacy  of  Rokitansky's  statements  concerning  the  an- 
tagonism between  mitral  stenosis  and  consumption.  It  is  worthy 
of  note,  however,  that  in  this  case  the  narrowing  was  not  extreme 
and  was  combined  with  regurgitation,  a  form  of  mitral  disease 
which  is  not  so  infrequently  associated  with  pulmonary  tubercu- 
losis as  was  once  thought. 

Furthermore,  this  case  raises  the  very  interesting  query  if 
this  stenosis  may  not  have  exerted  a  retarding  influence  upon  the 
progress  of  tho  lung  affection,  although  in  this  connection  it 
should  be  stated  that  her  residence  has  been  in  southwestern  Kan- 
sas, where  the  air  is  dry  and  the  altitude  not  far  from  2,000  feet. 


Fig.  52. — Location  of  Apex  and  Kelative 
DuLNESs  IN  Case  of  Mitral  Stenosis 
(p.  274). 


MITRAL  STENOSIS  277 

For  my  part  I  am  much  more  inclined  to  attribute  the  slow  ad- 
vance of  the  pulmonary  affection  in  this  case  to  other  factors, 
possibly  to  climatic  influences,  possibly  to  inherent  mildness  of 
the  tuberculous  infection  itself,  rather  than  to  the  mitral  obstruc- 
tion, since,  as  suggested  by  Sansom,  it  is  reasonable  to  assume  that 
a  valvular  lesion  would  have  a  tendency  to  impair  the  resistance 
of  the  organism,  particularly  in  one  inheriting  a  predisposition  to 
tuberculous  disease. 


CHAPTER    VIII 
AORTIC    REGURGITATION 

In  .this  form  of  valvular  disease  a  portion  of  the  blood  dis- 
charged into  the  aorta  with  each  ventricular  systole  leaks  back 
into  the  left  ventricle  during  its  diastole.  xVlthough  relative  in- 
competence may  be  produced  by  dilatation  of  the  aortic  ostium, 
the  disease  in  question  is  in  the  vast  majority  of  cases  due  to 
structural  defect  of  the  valve  itself. 

Morbid  Anatomy. — Defects  in  the  aortic  valve  leading  to 
regurgitation  are  as  nearly  analogous  to  those  found  in  mitral  re- 
gurgitation as  the  anatomy  of  the  valve  will  allow.  They  may 
follow  acute  endocarditis,  or  may  be  the  result  of  a  non-inflamma- 
tory sclerosis.  The  latter  is  more  often  the  case  here  than  at  the 
mitral  orifice  because  the  aortic  valve  has  to  bear  the  brunt  of 
the  increased  blood-pressure  due  to  muscular  exertion. 

The  leaflets,  one  or  all,  may  be  retracted,  curled,  or  shrivelled, 
so  as  to  permit  a  free  regurgitation.  Old  vegetations  on  the  ven- 
tricular surface  may  interfere  with  their  complete  apposition.  In 
short,  the  conditions  parallel  those  found  in  mitral  insiifiiciency, 
with  exception  of  the  influence  of  contraction  of  the  chordae  ten- 
dinese  and  papillary  muscles. 

Acute  incompetence  may  occur  during  ulcerative  endocarditis 
by  the  perforation  of  one  of  the  valve-cusps.  Very  rarely  a  cusp 
may  rupture  during  violent  muscular  exercise.  The  aortic  semi- 
lunar valve  is  one  of  the  most  delicate  structures  in  the  body,  and 
yet  one  of  the  strongest,  sustaining  as  it  does  the  Avhole  blood- 
pressure  of  the  systemic  circulation.  It  is  hence  extremely  un- 
likely that  muscular  exertion  could  be  severe  enough  to  raise 
blood-prcBsure  to  a  height  sufficient  to  rupture  a  healthy  valve. 
Probably  in  such  cases  the  valve  has  been  weakened  either  by  de- 
generation or  inflammation. 

As  in  mitral  disease,  regurgitation  is  often  combined  with 
278 


AORTIC  REGUEGITATION,  WITH  CALCIFIED  VEGETATION  THAT  SWUNG 
IN  BLOOD  CURRENT.  CAUSING  ATHEROMA  OF  ENDOCARDIUM  AND 
OF  INTIMA   OF   AORTA. 


AORTIC  REGURGITATION  279 

some  degree  of  stenosis,  but  regurgitation  may  occur  without  nar- 
rowing, and  occasionally,  in  consequence  of  dilatation  of  the  ven- 
tricle, even  with  stretching,  of  the  aortic  ring.  That  such  en- 
largement of  the  ring,  leading  to  relative  insufficiency,  could  take 
place,  was  long  doubted,  owing  to  the  great  strength  of  the  annulus 
iibrosus,  but  so  many  instances  of  the  kind  have  been  observed 
that  there  is  no  longer  any  room  for  doubt. 

The  first  effect  on  the  heart  is  dilatation  of  the  left  ventricle. 
This  is  due  to  the  impact  on  its  inner  surface  of  the  regurgitant 
stream, 'which  in  very  free  regurgitation  re-enters  with  nearly  the 
force  with  which  it  was  driven  out  of  the  ventricle.  Such  lesions, 
however,  are  of  gradual  development,  and  the  increasing  work 
leads  to  a  corresponding  hypertrophy  of  the  wall  of  the  ventricle, 
which  enables  it  not  only  to  withstand  the  strain  of  the  regurgita- 
tion, but  to  expel  the  greatly  increased  volume  of  blood  present  in 
the  chamber  at  the  beginning  of  its  systole.  This  hypertrophy  in 
aortic  insufficiency  is  of  early  development  and  often  becomes  so 
extreme  that  some  of  the  largest  hearts  on  record  are  those  show- 
ing this  defect.  The  wall  of  the  hypertrophied  ventricle  may  be 
as  thick  as  4  centimetres  (If  inch).  -  The  apex  of  the  left  ventricle 
projects  far  beyond  that  of  its  fellow,  and  the  interventricular 
sseptum  is  displaced,  encroaching  largely  on  the  cavity  of  the 
right  chamber. 

As  long  as  the  mitral  valve  remains  intact  the  effects  of  aortic 
regurgitation  upon  the  heart  are  limited  to  the  left  ventricle.  If, 
however,  the  mitral  is  incompetent,  either  from  disease  of  the 
valve  or  relatively  from  the  enlargement  of  the  ventricle,  the  phe- 
nomena described  as  the  results  of  mitral  incompetency  are  added 
to  those  of  the  aortic  lesion.  In  such  an  event,  of  course,  the  right 
heart  is  also  enlarged,  and  the  largest  hearts  have  been  those  show- 
ing this  combination  of  lesions.  Such  a  heart  may  weigh  as  much 
as  3  or  4  pounds.  Indeed,  von  Ziemssen  has  reported  6  pounds 
as  the  weight  of  a  specimen  obtained  from  one  of  the  great 
Stokes's  patients.  On  account  of  its  size  such  a  heart  is  spoken  of 
as  cor  hovinum.  The  heart  presented  to  me  by  Dr.  C.  C.  O'Byrne 
weighs  2|  pounds,  and  in  it  the  regurgitation  could  not  have  been 
extreme  (Plate  II).  The  point  of  interest  in  this  specimen  is  the 
swinging  vegetation,  3  centimetres  long,  and  containing  calcareous 
nodules,  which  evidently  swung  in  the  blood-stream,  now  in  the 


280  DISEASES   OF   THE   HEART 

ventricle,  and  again  in  the  aorta,  for  on  the  intima  of  the  aorta 
and  on  the  mural  endocardium  of  the  ventricle,  at  the  points 
where  the  vegetation  must  have  struck,  are  marked  atheroma- 
tous patches.  There  is  said  to  have  been  a  musical  murmur 
during  life. 

The  greatly  increased  force  with  which  such  a  ventricle  pro- 
pels the  blood  into  the  aorta  throws  great  strain  on  the  walls  of 
that  vessel,  and  hence  atheromatous  changes  are  often  found  not 
only  in  the  aorta,  but  in  the  whole  arterial  system.  That  such 
change  is  due  to  this  valvular  disease  is  indicated  by  the  fact 
of  its  occurrence  in  young  and  otherwise  healthy  individuals,  in 
whom  it  would  not  be  expected  to  exist. 

When  this  valvular  disease  is  the  result  of  a  general  sclerosis, 
the  myocardium  is  apt  to  be  so  degenerated  as  a  result  of  coronary 
involvement  that  hypertrophy  is  not  great.  It  is  when  the  disease 
develops  in  young  and  healthy  individuals  as  a  result  of  endocar- 
ditis that  the  enormous  heart  is  usually  found. 

Etiology. — Endocarditis  affecting  the  semilunar  valve  may 
have  the  same  origin  as  that  of  the  left  auriculo-ventricular  valve, 
and  hence  the  discussion  of  its  causes  does  not  need  to  be  repeated. 

Aortic  regurgitation  may  be  met  with  in  persons  of  both 
sexes  and  of  all  ages.  It  is  a  striking  fact,  however,  that  this 
lesion,  even  when  due  to  rheumatic  endocarditis,  is  far  more  com- 
mon in  males  than  in  females.  When  developed  at  or  after  mid- 
dle age,  it  is  usually  due  to  those  conditions  which  bring  about 
sclerosis,  and  which  are  fully  considered  in  other  chapters  (pages 
201  and  741).  This  sclerotic  form  is  also  undoubtedly  met  with 
more  frequently  in  males  than  in  females,  and  for  the  reason  that 
arterial  degeneration  is  more  common  in  the  former — and  there- 
fore the  etiological  factors  leading  to  sclerotic  change  in  the  aortic 
cusps  are  essentially  those  of  arteriosclerosis. 

In  a  considerable  portion  of  males  suffering  from  aortic  re- 
gurgitation there  is  a  history  of  syphilis  and  the  abuse  of  alco- 
hol. In  a  most  typical  case  of  this  lesion  recently  seen  in  a  man 
of  thirty-nine,  syphilis  and  whisky  were  the  only  two  causative 
factors  to  be  elicited.  Gout  and  bodily  toil,  particularly  if  com- 
bined with  alcoholic  excess,  also  seem  to  be  causative  agents  of 
considerable  importance. 

As  already  stated  incidentally  in   Morbid   Anatomy,   severe 


AORTIC  REGURGITATION  281 

strain  may  bring  about  acute  incompetence  of  one  of  the  aortic 
cusps  through  rupture  at  some  point  that  had  been  previously 
weakened  by  inflammation  or  atheromatous  degeneration. 

There  is  a  form  of  aortic  insufficiency  which,  although  not  due 
to  valvular  defect,  yet  presents  the  same  clinical  features  as  the 
organic  form,  and  is  so  frequently  encountered  that  it  may  here 
be  briefly  dwelt  upon.  This  is  a  relative  incompetence  of  the  semi- 
lunar valve,  and  its  causes  are  found  in  conditions  that  predis- 
pose to  stretching  of  the  ventricular  wall  and  of  the  basal  ring 
of  the  aorta.  They  are  therefore  (1)  degenerative  changes  in 
the  myocardium,  (2)  diseases  of  the  aorta  that  greatly  narrow 
its  lumen,  or,  per  contra,  lead  to  its  dilatation,  and  (3)  mediasti- 
nal tumours,  which  by  pressure  diminish  the  calibre  of  the  aorta. 
The  most  frequent  cause  of  this  relative  insufficiency  is  aneurysm 
affecting  the  ascending  arch,  or  a  general  dilatation  of  the  aorta 
secondary  to  sclerosis.  In  one  instance  of  the  latter  kind  coming 
under  my  notice  it  was  associated  with  mitral  regurgitation,  also 
of  atheromatous  type,  but  which  had  existed  for  years.  During 
the  later  weeks  of  life  in  this  case  aortic  incompetence  developed, 
and  after  death  was  found  due  to  extensive  atheromatous  degen- 
eration and  dilatation  of  the  aorta,  reaching  from  its  origin  to  the 
beginning  of  the  descending  portion  of  the  vessel. 

In  another  case  in  which  regurgitation  through  the  aortic 
valve  had  run  its  course  to  a  fatal  termination  within  a  few 
months,  post-mortem  examination  disclosed  stenosis  of  the  ascend- 
ing aorta,  about  I  an  inch  above  the  insertion  of  the  valve,  so 
pronounced  that  the  lumen  was  diminished  by  at  least  a  half. 
This  narrowing  was  caused  by  a  growth  of  fibrous  tissue  which 
completely  encircled  the  aorta,  and  from  the  history  appeared 
to  have  originated  in  acute  inflammation  a  year  and  a  half  pre- 
viously. 

As  already  stated,  relative  aortic  incompetence  may  be  the 
ultimate  effect  of  chronic  myocarditis,  which  is  associated  with 
sclerosis  of  the  aorta,  and  which  so  seriously  impairs  the  resist- 
ing power  of  the  ring  that  it  gradually  yields  to  the  distending 
force  of  the  blood-wave  as  it  recoils  against  the  closed  valve.  I 
have  seen  more  than  one  instance  of  the  kind  as  disclosed  by  the 
necropsy,  although  during  life  (he  regurgitation  had  been  attrib- 
uted to  structural  defect  of  the  valve-segments. 
20 


282  DISEASES  OP  THE   HEART 

Of  53  cases  of  aortic  regurgitation  of  wliicli  I  have  records,  46 
occurred  in  the  male  and  only  7  in  the  female  sex.  Seventeen  of 
the  males  and  -i  of  the  females  were  below  the  age  of  forty. 
Eleven  of  the  former  who  were  less  than  forty  years  of  age  gave  a 
history  of  rheumatism  or  scarlatina,  while  10  over  forty  also  had 
had  one  or  the  other  of  these  diseases.  Of  the  females,  2  below 
forty  and  1  over  that  age,  gave  a  history  of  rheumatism  or  scarla- 
tina. Of  the  total  number  of  cases,  therefore,  24  were  probably 
due  to  endocarditis.  It  may  also  be  stated  that  of  the  29  males 
and  3  females  over  forty  there  were  19  males  and  2  females  in 
whom  the  lesion,  owing  to  the  absence  of  probable  endocarditis, 
could  be  reasonably  attributed  to  atheroma.  In  whatever  way 
these  figures  are  looked  at  they  exhibit  the  striking  preponder- 
ance of  men  over  women  afflicted  with  this  particular  valve-defect. 

Symptoms. — It  goes  without  saying  that  in  this  as  in  other 
valvular  diseases  it  is  the  degree  of  compensation  which  deter- 
mines the  presence  or  absence  of  distinctively  cardiac  symptoms. 
In  other  words,  if  the  lesion  is  of  inflammatory  origin,  and  if  the 
state  of  the  myocardium  has  permitted  the  development  of  great 
hypertrophy,  the  disease  may  remain  entirely  latent  for  many 
years.  Arduous  occupations  requiring  great  physical  effort,  feats 
of  endurance  and  skill,  mountain-climbing,  running,  boat-racing, 
football  playing,  tennis,  etc.,  are  often  endured  without  discom- 
fort. I  recall  an  attorney  with  pronounced  aortic  insufficiency  of 
rheumatic  origin  who  consulted  me  soon  after  his  return  from  a 
six-weeks'  vacation  in  Colorado.  He  had  ridden  his  wheel  at  an 
altitude  of  6,000  feet  with  no  more  discomfort  than  he  would 
have  experienced  in  Chicago.  The  only  time  he  had  suffered  any 
inconvenience  was  when  he  had  taken  the  train  up  Pike's  Peak. 
Upon  reaching  the  summit,  13,000  feet,  he  fainted  away,  yet 
upon  returning  to  the  foot  of  the  mountain  he  got  on  his  wheel 
and  rode  away  as  if  nothing  had  happened. 

Dyspnoea  is  not  experienced  in  this  stage,  and  aside  from  vio- 
lent action  of  the  heart,  patients  are  totally  unconscious  that  the 
organ  is  anywise  different  from  that  of  their  fellows.  If  any  dis- 
turbance of  bodily  function  exists,  it  is  not  such  as  arises  from 
venous  congestion,  for  so  long  as  the  mitral  valve  remains  com- 
petent stasis  back  of  the  left  ventricle  is  impossible. 

The  state  of  the  circulation  is  one  of  intermittent  anaemia  on 


AORTIC   REGURGITATION  283 

the  part  of  the  arterial  system.  At  each  systole  the  arteries  are 
flushed,  and  with  each  diastole  they  are  relatively  depleted.  The 
tendency,  therefore,  is  to  a  lack  of  nutrition  of  the  various  organs 
and  tissues  throughout  the  body.  This  is  not  specially  manifest 
in  some  persons,  while  in  others  there  is  more  or  less  pallor  and 
delicacy  of  body.  The  muscular  system  in  particular  is  weak, 
and  some  children  show  inability  for  sustained  mental  effort,  yet 
as  a  rule  young  persons  with  aortic  regurgitation  show  nothing 
either  in  appearance  or  deportment  to  indicate  the  existence  of 
their  lesion. 

A  well-compensated  aortic  insufficiency  is  not  likely  to  inca- 
pacitate an  otherwise  healthy  young  adult  for  the  active  and  even 
the  arduous  duties  of  professional  or  mercantile  pursuits.  Many 
a  hard- worked  medical  man  with  this  lesion  is  able  to  sustain  the 
severe  mental  and  physical  strain  of  a  large  general  practice  with- 
out more  fatigue  than  his  more  fortunate  confreres.  The  only 
symptoms  experienced  by  some  patients  are  palpitation  or  slight 
vertigo,  or  both,  and  yet  trivial  as  they  may  seem  to  be  they  are 
sometimes  the  earliest  announcement  of  faltering  energy  on  the 
part  of  the  left  ventricle.  In  one  instance,  more  than  twenty 
years  before  the  patient's  death,  any  effort  or  excitement  beyond 
a  certain  moderate  degree,  brought  on  attacks  of  such  violent  pal- 
pitation as  to  necessitate  absolute  repose  for  hours  in  the  recum- 
bent posture.  These  attacks  were  also  produced  by  even  small 
doses  of  digitalis,  and  as  they  were  allayed  by  aconite  they  were 
thought  due  to  extreme  hypertrophy.  In  most  cases  such  violent 
cardiac  action  is  an  expression  of  weakness  rather  than  of  ex- 
cessive strength,  as  sometimes  supposed.  When  dizziness  is  expe- 
rienced, it  is  usually,  though  by  no  means  always,  induced  by 
sudden  exertion,  and  in  such  cases  it  is  generally  found  that  the 
regurgitation  is  very  free. 

The  cerebral  arteries  are  flushed  w^ith  each  systole,  but  in 
consequence  of  the  regurgitation  blood-pressure  wdthin  them  is 
not  sustained,  and  when  for  any  reason  the  reflux  into  the  ven- 
tricle is  intensified,  transient  anaemia  of  the  brain  results  and 
vertigo  is  felt.  In  some  cases  dizziness  is  produced  by  intermit- 
tence  in  the  heart's  contractions,  and  it  is  then  a  mild  manifesta- 
tion of  what  in  other  cases  becomes  a  syncopal  attack.  Indeed, 
fainting  is  an  occasional  symptom  in  this  disease,  in  consequence 


284  DISEASES   OF   THE   HEART 

of  the  fact  that  the  state  of  the  cerebral  circulation  is  the  opposite 
of  what  obtains  in  mitral  stenosis.  This  explains,  I  think,  why  it 
is  that  aortic  patients  are  able  to  lie  low  in  bed,  whereas  those 
suffering  from  mitral  disease  usually  prefer  to  sleep  with  their 
head  and  shoulders  propped  up  on  two  pillows.  In  the  former 
there  is  an  unconscious  attempt  to  overcome  the  force  of  gravita- 
tion upon  the  cerebral  circulation,  while  the  latter  class  of  patients 
seek  to  aid  venous  flow  out  of  the  head  by  that  same  force  of  gravi- 
tation. 

Disorders  of  digestion  are  not  so  common  in  aOrtic  as  in  mitral 
patients,  and  when  present  are  referable  not  to  interference  with 
the  circulation,  as  has  been  explained  is  the  case  in  lesions  at  the 
auriculo-ventricular  orifice,  but  they  are  due  in  most  instances  to 
errors  in  diet  or  whatever  deranges  gastro-intestinal  function  in 
individuals  who  have  no  heart-disease. 

The  comparative  immunity  from  symptoms  enjoyed  for  years, 
it  may  be,  by  persons  whose  disease  is  the  result  of  endocarditis, 
is  not  the  fortunate  lot  of  those  in  whom  the  aortic  valves  have 
become  incompetent  in  consequence  of  sclerosis,  and  in  whom  the 
myocardium  is  incapable  of  maintaining  adequate  compensatory 
hypertrophy.  In  persons,  therefore,  whose  signs  of  aortic  regurgi- 
tation develop  during  middle  age,  symptoms  are  apt  to  appear 
early  and  to  be  pronounced.  These  do  not  differ  essentially  from 
those  experienced  by  patients  of  the  other  class,  and  are  palpita- 
tion, vertigo  of  more  or  less  intensity  and  frequency,  a  feeling  of 
general  weakness,  uncomfortable  pr?ecordial  oppression,  more  or 
less  pain  that  may  be  distinctly  anginal  or  of  an  anginoid  char- 
acter, and  in  particular  distressing  attacks  of  dyspnoea.  When 
these  symptoms  arise  a  fatal  termination  is  not  far  distant. 

With  Dr.  G.  W.  Webster,  October  13,  1900,  I  saw  an  Irishman 
who  presented  a  very  striking  picture  of  the  distress  often  experi- 
enced in  the  terminal  stage  of  aortic  incom])etence.  There  was  no 
history  of  inflammatory  rheumatism,  but  of  syphilis  and  the  im- 
moderate use  of  alcohol.  Three  weeks  prior  to  my  visit  he  had  been 
in  the  country,  and  while  there  had  overexerted  himself,  become 
greatly  fatigued,  and  had  begnn  to  suffer  from  attacks  of  sudden 
weakness  with  a  feeling  of  suffocation.  Upon  his  admission  to 
the  hospital  he  was  suffering  from  frequent  attacks  that  seemed 
to    portend    speedy    dissolution.       llis    hurried    and    somewhat 


AORTIC   REGURGITATION 


285 


laboured  respirations  would  suddenly  become  so  augmented  in 
severity  that  he  would  spring  into  the  upright  position  gasping 
for  breath,  coughing  and  raising  frothy  mucus,  while  cyanosis 
became  marked,  and  the  pulse  grew  rather  more  rapid,  irregular, 
and  extremely  feeble.  The  face  became  anxious,  and,  in  a  word, 
the  whole  appearance  of  the  man  was  one  of  direst  distress.  The 
examination  on  admission  disclosed  aortic  regurgitation  and  a 
secondarily  leaking  mitral,  with  very  swollen  and  tender  liver. 
Hypodermics  of  morphine  relieved  these  attacks  in  a  measure, 
and  under  the  free  use  of  cathartics,  digitalis  and  iodide  of  soda, 
the  condition  so  much  improved  that  the  mitral  no  longer  leaked. 
I  found  a  rather  spare  man  of  medium  stature  who  looked 
much  older  than  he  really  was.  He  was  semi-recumbent,  and 
although  comfortable  was  yet  breathing  with  apparent  difficulty 
and  greater  than  normal  rapidity.  There  was  no  oedema,  and 
signs  of  stasis  were  not  notice- 
able. The  temporal  and  cervi- 
cal arteries  throbbed  strongly, 
the  pulse  was  quick  and  of 
the  character  known  as  bis- 
feriens,  and  the  radial  arteries 
were  stiff.  The  lower  border 
of  the  liver  was  palpable  a 
short  distance  below  the  costal 
arch,  but  the  organ  was  not 
hard  or  tender.  Cardiac  im- 
pulse was  diffused  and  weak, 
the  indistinct  broad  apex-beat 
being  in  the  sixth  interspace, 
midway  between  the  left 
mamillary   and   anterior   axil-      fig.  53— Location  of  Apex  and  Kelative 

lary  lines.     Percussion  showed  Durness,  Case  of  Aortic  Insufficiency 

slight      increase      01      cardiac 

dulness  to  the  right  of  the  sternum  and  downward,  but  very 
great  extension  of  dulness  towards  the  left  and  downward.  The 
outer  border  was  broadly  rounded,  after  the  manner  often  de- 
scribed as  indicative  of  preponderating  dilatation  of  the  left  ven- 
tricle in  cases  of  aortic  insufficiency  with  broken  compensation 
(Fig.   53).     When  hypertrophy  predominates,  the  outline  of  the 


286  DISEASES  OF   THE   HEART 

left  Yentricle  is  long  and  pointed  with  a  rather  sharp  apex.  Upon 
ansciiltation  there  was  at  once  detected  a  systolic  and  diastolic 
murnuir  of  the  usual  character  in  aortic  regurgitation,  but  with 
the  exception  of  the  accentuated  pulmonic  second  tone  the  heart- 
sounds  were  scarcely  audible.  Indeed,  the  aortic  second  was 
quite  wanting,  and  in  the  neck  was  replaced  by  the  feeble  dis- 
tant diastolic  bruit.  At  the  seat  of  the  apex  the  ear  perceived 
a  dull  or  toneless  thud  rather  than  the  normal  first  sound,  and  the 
diastolic  murmur  was  faintly  distinguishable.  In  the  femoral 
artery,  pressure  elicited  the  double  murmur  of  Duroziez. 

The  diagnosis  was  easy  enough.  It  was  an  aortic  regurgita- 
tion of  atheromatous  origin  in  the  stage  of  ruptured  compensa- 
tion that  had  led  to  venous  stasis.  The  congestion  of  the  lungs 
was  shown  by  the  frequent  cough  and  sero-mucous  sputum,  and 
the  stasis  in  the  general  system  by  the  hepatic  enlargement  and 
scanty  urine.  The  patient  was  unable  to  sleep,  and  the  taking 
of  food  was  followed  by  the  formation  of  gas,  which  contributed 
its  quota  to  the  already  existing  dyspnoea. 

The  prognosis  was  of  the  worst,  for  it  was  only  too  evident 
that  the  left  ventricle  could  not  withstand  the  impact  of  the  regur- 
gitating stream.  That  this  was  free  was  shown  by  the  absence  of 
the  aortic  second  sound^  which  had  become  wholly  replaced  by  the 
diastolic  murmur.  The  attacks  of  increased  dyspna^a  and  cardiac 
feebleness  were  the  manifestation  of  left  ventricle  failure  or  asys- 
tolism  and  portended  grave  danger.  In  fact,  although  as  vigor- 
ous and  skilful  treatment  was  maintained  as  could  be  devised,  it 
exercised  no  appreciable  effect  on  the  patient's  condition,  and 
after  lingering  another  five  days  he  expired  in  one  of  his 
attacks. 

There  is  a  twofold  reason  why  aortic  regurgitation  of  the 
sclerotic  type  is  particularly  serious.  Xot  only  has  more  or  less 
myocardial  degeneration  preceded  the  development  of  the  valvu- 
lar defect,  but  the  reflux  of  a  portion  of  the  contents  of  the  aorta 
into  the  left  ventricle  augments  the  cardiac  ischa'mia  resulting 
from  the  aortic  and  often  coexisting  coronary  sclerosis.  I  will 
not  discuss  the  much-debated  question  whether  the  coronary  arter- 
ies are  fluslied  during  systole  or  diastole,  since  this  is  amply  set 
forth  in  works  on  physiology,  but  only  state  that  the  weight  of 
evidence  is  in  favour  of  tlie  svstolic  flushinc  of  the  heart-muscle. 


AORTIC  REGURGITATION  287 

It  is  sufficient  to  emphasize  tlie  fact  that  in  aortic  regurgitation 
blood-pressure  is  not  sustained  within  the  coronary  any  more  than 
in  other  arteries,  and  hence  cardiac  nutrition  cannot  be  good. 

There  comes  at  length  a  limit  in  all  cases  to  cardiac  hyper- 
trophy because  the  heart-muscle  becomes  more  or  less  degenerated, 
and  therefore  incapable  of  maintaining  the  circulation  and  of 
withstanding  the  dilating  force  of  the  regurgitant  stream.  Its 
flagging  energy  is  shown  by  more  rapid  and  perhaps  less  regular 
contractions,  even,  it  may  be,  by  occasional  intermissions. 

Therefore,  the  earliest  and  most  reliable  indications  of  failing 
compensation  are  generally  sho^vn  in  the  pulse.  Even  before  sub- 
jective symptoms  bring  the  patient  to  his  medical  adviser  the 
pulse-waves  are  no  longer  of  uniform  frequency,  force,  and  vol- 
ume. The  radial  pulse  is  accelerated,  but  it  does  not  strike  the 
j)alpating  finger  with  its  old-timed  suddenness  and  vigour,  the 
artery  not  being  so  powerfully  and  quickly  distended  as  when  the 
ventricle  contracts  with  energy.  Consequently  the  physician  may 
not  so  readily  distinguish  the  peculiar  characters  of  the  aortic  re- 
gurgitant pulse.  At  irregular  intervals  the  pulse  seems  to  falter 
a  little,  or  a  small,  weak  beat  follows  its  predecessor  more  quickly 
than  usual,  and  is  followed  by  others  of  normal  strength. 

This  is  the  expression  of  an  accessory  or  extra  systole,  intro- 
duced now  and  then  into  the  regular  series  of  contractions  for 
the  purpose  of  re-enforcement  (pulsus  intercurrens),  or  it  is  the 
result  of  the  ventricle  giving  a  hurried,  incomplete  contraction, 
in  consequence  of  fatigue.  As  muscular  incompetence  increases, 
the  pulse  grows  more  irregular,  or  indeed  becomes  permanently 
intermittent.  It  increases  in  frequency,  and  its  distinctive  collaps- 
ing character,  to  be  subsequently  described,  grows  less  apparent. 

Subjective  symptoms  annoy  or  even  alarm  the  patient,  who 
begins  to  notice  an  unwonted  breathlessness.  Attacks  of  vertigo 
or  even  syncope  supervene.  If  the  patient  does  not  now  die  sud- 
denly and  unexpectedly,  he  is  likely  to  suffer  from  irregularly  re- 
curring attacks  that  are  of  grave  danger  because  indicating  immi- 
nent cardiac  paralysis.  These  are  a  more  or  less  sudden  feeling 
of  great  weakness  or  prostration,  with  cyanosis,  a  feeble,  irregu- 
lar, perhaps  accelerated  and  empty  pulse,  dyspnoea,  and  an  inde- 
scribable feeling  of  impending  dissolution.  In  addition,  he  may 
suffer  from  cough  with  frothy,  it  may  be  bloody,  expectoration 


288  DISEASES  OP  THE  HEART 

and  other  symptoms  indicative  of  stasis  in  the  jmlmonarv  vessels 
and  general  venous  system.  If  the  mitral  valve  has  become  rela- 
tively incompetent,  regurgitation  through  the  auriculo-ventricu- 
lar  opening  is  added  to  that  already  present  at  the  aortic  orifice, 
and  the  sjanptoms  become  the  same  as  those  of  the  last  stages  of 
mitral  disease. 

Early  in  my  practice  I  was  called  to  attend  a  middle-aged 
woman,  whom  I  found  intensely  dropsical^  ortliopnocic,  and  pre- 
senting unmistakable  evidence  of  aortic  and  relative  mitral  insuf- 
ficiency. Rest  in  bed,  infusion  of  digitalis  and  catharsis  speedily 
removed  the  anasarca,  closed  up  the  mitral  valves,  and,  in  short,  so 
greatly  improved  her  condition  that  she  thought  herself  fully  re- 
stored. Despite  my  warning,  and  contrary  to  my  strict  orders, 
she  insisted  upon  leaving  her  bed  and  sitting  dressed  in  the  family 
living  room.  Only  a  day  or  two  thereafter,  while  alone  in  her 
apartment,  she  lieard  a  rap  on  the  door,  arose  quickly  to  answer 
the  knock,  opened  the  door,  and  almost  immediately  fell  to 
the  floor  and  died.  In  this  case  I  believe  life  might  have  been 
prolonged  had  the  mitral  valves  continued  to  leak,  and  thus  acted 
as  a  safety-valve  for  the  left  ventricle. 

I  am  led  to  this  opinion  by  my  observation  of  a  case  with  Dr. 
Lowrence  at  Chebanse,  111.  The  patient  was  an  old  man,  who  was 
suffering  from  albuminuria,  dropsy,  congested  liver,  and  orthop- 
noea.  Upon  examination,  there  were  the  usual  signs  of  stiffened 
arteries  and  aortic  regurgitation,  but,  in  addition,  a  mitral  regur- 
gitant murmur,  pulsation  of  the  external  jugulars,  and  a  murmur 
characteristic  of  tricuspid  insufficiency.  I'he  outlook  seemed  very 
bad,  and  but  small  hope  for  improvement  was  held  out.  Never- 
theless, upon  the  daily  moderate  use  of  cathartics  and  nitro- 
glycerin, tlio  replacement  of  digitalis  by  strophanthus,  and  the 
hypodermic  administration  of  small  tonic  doses  of  morphine,  this 
patient  actually  improved  beyond  all  expectation,  and  several 
months  subsequently  was  reported  by  the  doctor  as  still  alive 
and  in  tolerable  comfort,  being  able  to  drive  out  in  pleasant 
weather,  although,  needless  to  say,  compensation  was  never  re- 
stored. I  believe  in  this  instance  the  leakage  of  the  mitral  and 
tricuspid  valves  relieved  the  two  ventricles  from  dangerous  strain 
and  threw  the  brunt  of  the  trouble  back  upon  the  liver  and  general 
venous  system.     The  stasis  thus  resulting,  of  course,  produced  res- 


AORTIC  REGURGITATION  289 

piratory  embarrassment  and  functional  derangement  of  the  ab- 
dominal viscera,  but  actually  served  to  prolong  life. 

In  my  care  in  the  wards  of  Cook  County  Hospital  there  are 
at  the  present  writing  two  men  with  aortic  regurgitation  in  whom 
mitral  incompetence  has  become  added.  Both  present  evidence 
of  venous  stasis  in  a  moderate  degree,  chiefly  hepatic  and  pulmo- 
nary. One  complains  of  weakness  and  but  little  else,  the  other  of 
insomnia ;  yet  in  both  patients  things  are  growing  slowly  worse  in 
spite  of  rest  in  bed  and  the  usual  heart-tonics.  To  all  intents  and 
purposes  they  have  become  converted  into  cases  of  mitral  disease, 
the  most  frequent  sequel  of  events  in  aortic  regurgitation.  The 
chief  difference,  however,  lies  in  the  refractoriness  to  treatment 
and  in  the  liability,  one  might  almost  say  certainty,  of  a  sudden 
death. 

In  June,  1899,  I  saw  with  Dr.  Houston  a  powerfully  built 
Irishman,  weighing  over  200  pounds,  Avho  was  suffering  from 
dyspnoea,  which  had  suddenly  developed  six  weeks  previously. 
His  personal  history  was  negative  with  exception  of  swelling  of 
one  knee  some  six  or  eight  years  before.  This  may  have  been  a 
monarticular  rheumatism^  and  if  so,  it  may  have  been  responsible 
for  the  man's  valvular  disease.  It  was  not  followed  by  any  symp- 
toms, for  with  exception  of  a  fall  that  occasioned  pain  near  the 
heart  for  a  day  he  had  been  perfectly  well  up  to  his  present  ill- 
ness. No  history  of  overexertion  or  any  other  exciting  cause  for 
his  dyspnoea  could  be  elicited.  His  shortness  of  breath  had  set  in 
abruptly  while  he  was  attending  his  duties  as  engineer,  and  at 
first  had  been  more  severe  than  it  was  when  I  saw  him,  the  im- 
provement being  due  to  treatment,  l^evertheless  he  was  incapaci- 
tated for  work,  and  counsel  was  sought  in  the  hope  of  obtaining 
some  suggestion  for  his  further  improvement. 

The  pulse  was  arrhythmic  and  rapid,  displaying  feebly  the 
usual  characters  of  aortic  insufficiency,  and  the  vessels  did  not 
feel  thickened  and  stiff.  The  broad,  heaving  apex-impulse  was 
displaced  downward  into  the  sixth  interspace  and  outward  to  the 
anterior  axillary  line.  There  was  epigastric  pulsation  and  a  sys- 
tolic thrill  in  the  aortic  area.  The  heart-tones  were  everywhere 
audible,  though  feebly,  and  there  was  a  loud,  rough  systolic  mur- 
mur at  the  base  to  right  of  sternum,  followed  by  a  very  feeble 
diastolic  bruit.     At  the  apex  could  be  made  out  a  softer  systolic 


290  DISEASES   OF  THE  HEART 

murmur  possessing  the  characters  of  a  mitral  regurgitant  one, 
which,  together  with  evidences  of  enlargement  of  the  right  heart, 
convinced  me  that  the  mitral  as  well  as  the  aortic  valves  were 
leaking.  The  liver  was  palpahle  and  tender,  and  the  urine  con- 
tained a  small  amout  of  albumin.  I  looked  upon  the  mitral  insuf- 
ficiency as  relative  and  secondary  to  the  aortic  disease. 

The  prognosis  was  very  unfavourable,  notwithstanding  the 
degree  of  improvement  that  had  already  attended  treatment,  be- 
cause when  compensation  is  once  lost  in  this  form  of  valvular 
disease  it  is  rarely  possible  to  restore  the  dilated  and  perhaps  de- 
generated left  ventricle  to  its  former  vigour. 

The  patient  was  informed  of  his  grave  state,  and  was  advised 
to  keep  his  room  for  as  long  a  time  as  was  thought  best,  the  dura- 
tion to  be  determined  by  results.  In  addition  to  rest,  the  treat- 
ment was  to  consist  of  strychnine,  digitalis,  and  nitroglycerin ; 
food  was  to  be  light  but  sustaining,  and  cathartics  were  to  be 
employed  daily,  but  not  enough  to  weaken  him.  The  purpose  of 
the  last-named  remedies  was  chiefly  to  prevent  the  patient  from 
being  obliged  to  strain  at  stool,  as  might  be  the  case  were  he  to 
become  at  all  constipated.  It  is  well  known  that  effort  of  this 
kind  is  particularly  bad,  even  dangerous,  for  persons  whose  left 
ventricle  is  in  a  state  of  dilatation.  In  aortic  regurgitation  the 
sudden  constriction  of  the  arteries  incident  to  straining  is  liable 
to  cause  sudden  and  fatal  diastolic  arrest  of  the  heart. 

In  October  I  saw  the  patient  again,  and  was  not  surprised, 
although  disappointed,  to  find  that  in  spite  of  treatment  the  dila- 
tation of  the  left  ventricle  and  resulting  insufficiency  of  the  mitral 
valves  had  increased.  The  action  of  the  heart  was  more  regular, 
but  in  other  respects  things  had  grown  rather  more  ominous.  lie 
was  now  ordered  to  keep  his  bed  strictly,  and  was  put  on  larger 
doses  of  digitalis.  Improvement  did  not  follow,  and  he  began  to 
suffer  much  from  sudden  paroxysms  of  dyspna3a,  which  were 
very  alarming  to  him  and  his  friends.  His  liver  also  became 
greatly  engorged,  and  his  whole  condition  grew  steadily  more 
threatening.  Strychnine  and  nitroglycerin  were  increased,  and 
he  was  given  daily  injections  of  morphine,  -J  of  a  grain,  with 
atropine  to  lessen  dypsnoea,  quiet  his  nervousness,  and  sustain  his 
heart. 

It  was  decided  to  persevere  in  the  use  of  digitalis,  interrupt- 


AORTIC  REGURGITATION  291 

ing  it  from  time  to  time  and  substituting  therefor  tincture  of 
strophantlius,  to  prevent  the  possible  cumulative  action  of  the  fox- 
glove. This  was  carried  out  until  at  length  a  singular  mental 
state  developed,  characterized  by  delusions  closely  resembling  a 
mild  mania.  As  Dr.  Houston  had  observed  a  similar  mental 
state  once  before  in  a  patient  whom  I  had  turned  over  to  his 
charge,  and  in  that  instance  had  discovered  it  was  caused  by 
digitalis,  he  concluded  it  was  of  the  same  nature  and  origin  in 
this  case  and  promptly  stopped  the  drug.  As  in  the  other  case, 
so  also  in  this,  the  delusions  and  other  maniacal  manifestations 
lasted  about  twenty-four  hours,  and  then  disappeared  entirely; 
This  rare  effect  of  the  prolonged  administration  of  this  agent  will 
be  spoken  of  in  the  chapter  on  Treatment  of  Valvular  Diseases. 

Patient  was  seen  again  in  January.  He  was  still  in  bed, 
where  he  had  remained  since  the  fore  part  of  October,  was  quite 
recumbent,  and  breathing  tranquilly,  although  he  stated  he  had 
occasional  paroxysms  of  dyspnoea  that  compelled  him  to  spring 
up  for  breath.  These  spells  of  difficult  breathing  had  returned 
upon  him  about  the  1st  of  January  after  a  period  of  constipa- 
tion. His  physician  stated  that  as  a  result  of  vigorous  purgation, 
digitalis,  strychnine,  and  morphine  hypodermically,  and  restricted 
diet,  which  was  kept  up  for  nearly  two  months,  his  condition  had 
by  late  autumn  improved  wonderfully.  The  enlarged  liver  had  re- 
turned nearly  to  normal,  his  colour  had  grown  quite  natural,  and 
his  pulse  stronger,  of  better  volume,  and  regular,  the  heart-sounds 
stronger,  and  the  apex-beat  fairly  well  defined.  Recently,  how- 
ever, the  patient  had  become  intolerant  of  the  cathartics  and  pro- 
longed rest  in  bed,  and  had  implored  to  be  allowed  to  sit  up. 

I  found  the  pulse  about  70,  with  two  intermissions  in  a  min- 
ute and  a  half,  but  very  compressible,  and  its  collapsing  character 
not  well  marked.  The  liver  was  palpable,  particularly  the  left 
lobe,  which  was  very  tender  in  the  epigastrium.  There  was  no 
oedema,  although  the  feet  were  a  little  puffy.  Cardiac  impulse 
was  wanting  except  for  an  occasional  vague  apex-beat  consider- 
ably outside  the  left  nipple  in  the  sixth  interspace.  Heart's  dul- 
ness  was  pronounced,  presenting  in  this  regard  a  marked  contrast 
to  its  condition  in  October,  when  it  was  obscured  by  pulmonary 
resonance.  It  was  of  triangular  outline,  reaching  to  the  third 
interspace,  and  from  2  inches  to  right  of  sternum  across  nearly 


292  DISEASES  OF  THE  HEART 

to  the  left  anterior  axillary  line,  well  outside  of  the  occasionally 
])alpable  impulse.  The  lungs  were  eyerywhere  resonant.  The 
heart-sounds  were  audible  though  faint,  the  aortic  second  being 
particularly  feeble,  and  the  pulmonic  second  accentuated.  A  loud, 
harsh  murmur  was  present  throughout  the  pra^cordium,  which  was 
systolic,  but  could  not  be  traced  to  any  particular  area.  Oyer  the 
body  of  the  organ  it  disappeared  on  firm  pressure,  permitting  other 
more  distant  and  persistent  murmurs  to  be  distinguished.  These 
were  found  to  be  a  harsh  aortic  systolic,  a  soft  mitral  systolic 
transmitted  to  the  back,  and  a  feeble  diastolic,  which  was  of  aortic 
origin,  as  shown  by  its  area  of  intensity  and  direction  of  propa- 
gation. 

The  diagnosis  was  apparent;  added  to  his  old-standing  aortic 
insuificiency  with  relatiye  mitral  regurgitation  there  was  a  peri- 
carditis with  moderate  effusion.  The  liyer  was  both  congested 
and  displaced  downward. 

The  prognosis  was  most  unfavourable,  for  in  addition  to  the 
cardiac  dilatation  depending  largely  on  myocardial  degeneration, 
a  pericarditic  effusion  had  taken  place.  As  is  well  known,  this 
sometimes  superyenes  upon  a  chronic  valvular  disease,  particu- 
larly aortic  insufficiency,  and  is  then  apt  to  be  a  terminal  event. 
It  was  stated  to  the  family  that  sudden  death  was  not  improbable. 

In  the  way  of  treatment,  compound  cathartic  pills  were  or- 
dered, the  patient  objecting  to  elaterium  and  disagreeable  saline 
waters ;  digitalis  in  considerable  doses,  a  grain  of  codeine  thrice 
daily  to  promote  quiet  and  to  lessen  the  paroxysms  of  dyspncea, 
and  restricted  diet.  Morphine  was  not  prescribed  because  of  its 
constipating  and  other  objectionable  effects. 

In  spite  of  the  greatest  possible  care  this  ])atient  did  not  im- 
prove, and  one  month  later  died  suddenly  and  quietly  M'hile  rest- 
ing in  bod,  as  usual.  This  case  not  only  portrays  the  clinical  pic- 
ture often  seen  in  aortic  regurgitation,  but  also  illustrates  the 
powerlessness  of  our  art  in  attempting  to  stay  the  progress  of  the 
disease. 

In  this  and  Dr.  Webster's  case  there  was  one  symptom  com- 
mon to  both — i.  e.,  paroxysmal  dyspnd'a.  In  the  one  case  it 
seemed  due  to  sudden  threatening  asystolism  of  the  left  ventricle, 
as  shown  by  feebleness,  rapidity,  and  irregularity  of  the  pulse,  and 
pulmonary  congestion,  manifested  by  cough  and  frothy  expectora- 


AORTIC  REGURGITATION  293 

tion.  In  the  other  there  was  also  threatening  weakness  of  the 
heart's  action,  but  the  striking  concomitant  was  the  intense  anx- 
iety amounting  to  fear,  so  that  the  patient  would  spring  up  in 
bed  gasping  for  breath  and  looking  wild  and  terrified.  In  both 
these  instances,  moreover,  the  symptoms  of  cardiac  breakdown  de- 
veloped suddenly,  and  were  never  again  wholly  lost,  in  this  re- 
spect differing  markedly  from  the  gradual  onset  of  compensatory 
failure  seen  in  mitral  affections.  In  both  cases  mitral  regurgita- 
tion Avas  superadded,  but  instead  of  the  end  coming  with  pro- 
nounced dropsy  death  was  sudden,  before  venous  stasis  progressed 
to  that  degree. 

In  my  experience  young  persons  who  have  contracted  their 
aortic  insufficiency  in  consequence  of  endocarditis  rarely  suffer 
from  cardiac  pain,  while,  on  the  other  hand,  I  have  observed 
numerous  instances  of  angina  pectoris  in  individuals  whose  aortic 
lesion  had  resulted  from  degenerative  changes.  In  1891  I  began 
to  treat  a  married  woman  of  about  thirty  who  was  afflicted  with 
aortic  incompetence  and  attacks  of  precordial  pain.  She  was 
quite  stout,  and  this  made  examination  of  the  heart  difficult.  The 
radial  pulse  was  collapsing,  though  not  as  full  and  quick  as  in 
typical  cases,  and  she  had  an  aortic  regurgitant  murmur.  The 
apex-beat  could  not  be  distinctly  made  out,  and  the  large  breast 
prevented  my  determining  the  boundary  of  deep-seated  dulness  at 
the  left.  The  absence  of  manifest  cardiac  hypertrophy  rather 
puzzled  me,  but  eventually  led  me  to  conclude  that  the  leak  was 
not  very  free,  and  consequently  that  there  was  not  much  hyper- 
trophic dilatation  of  the  left  ventricle.  After  she  had  been  under 
treatment  for  a  time  she  called  attention  to  a  pulsation  in  the  neck. 
This  was  found  to  be  just  behind  and  above  the  right  sterno-cla- 
vicular  articulation  in  the  location  of  the  innominate  artery.  It 
was  attributed  to  aneurysm  of  the  arch  of  the  aorta,  which  thus 
brought  the  innominate  prominently  into  view.  The  patient  was 
taken  to  several  diagnosticians  for  opinion,  and  among  others  to 
the  late  Dr.  Christian  Fenger,  by  whom  my  diagnosis  was  con- 
firmed. This  discovery  of  a  probable  aneurysm  changed  my  views 
concerning  the  etiology  and  pathology  of  the  case.  Whereas  the 
history  had  led  me  to  regard  the  aortic  regurgitation  as  of  rheu- 
matic origin,  I  now  considered  it  secondary  to  aortic  aneurysm, 
a  view  that  seemed  to  account  for  the  attacks  of  angina. 


294  DISEASES  OF  THE  HEART 

The  patient  then  left  Chicago,  and  I  did  not  see  her  for  sev- 
eral years.  At  length  I  was  one  day  nnexpectedly  summoned  to 
visit  her  at  one  of  the  hotels  to  which  she  had  betaken  herself 
immediately  upon  her  return  from  Europe  the  day  before.  She 
was  in  a  truly  pitiable  plight.  The  attacks  of  agonizing  pain  had 
become  so  frequent  and  severe  that  she  literally  could  not  walk 
across  the  room  without  one  being  evoked,  and  she  was  taking 
large  doses  of  nitroglycerin  and  whisky,  though  with  but  slight 
eifect.  The  circumference  of  the  neck  was  greater  than  normal, 
although  the  evident  congestion  had  not  produced  a-dema.  The 
old-time  pulsation  was  still  in  evidence.  It  did  not  appear  to 
have  increased  in  area,  and  the  only  alteration  I  could  detect  in 
the  heart-findings  was  greater  rapidity  and  feebleness  of  action. 
She  was  given  injections  of  morphine  sufficient  to  somewhat  blunt 
her  sensibility  to  pain,  but  aside  from  this  there  was  nothing  that 
could  be  done.  She  dragged  out  a  miserable  existence  for  a  few 
weeks  longer,  and  then  in  one  of  her  attacks  death  mercifully 
ended  her  sufferings. 

At  the  autopsy,  which  was  performed  by  Dr.  Frank  S.  John- 
son, who  had  also  seen  the  case,  the  aortic  valves  were  found  very 
incompetent  and  sclerotic,  but  whether  the  process  had  originally 
been  of  endocarditic  origin  or  not  it  was  difficult  to  decide.  There 
was  a  moderate  degree  of  enlargement  of  the  left  ventricle,  the 
walls  of  which  were  fatty.  The  two  most  interesting  features, 
however,  were  (1)  occlusion  of  the  mouths  of  the  coronary  arter- 
ies by  deposits  of  lime-salts,  so  that  they  with  difficulty  admitted 
the  point  of  a  fine  probe,  and  (2)  the  size  of  the  aorta.  Xo  aneu- 
rysm could  be  detected,  but  careful  measurement  showed  that  the 
ascending  portion  of  the  arch  was  uniformly  increased  in  diam- 
eter by  about  1  centimetre,  while  its  walls  were  possibly  a  trifle 
thinner  than  normal.  It  seemed  probable,  therefore,  that  when 
distended  by  the  abnormally  large  blood-wave  it  became  stretched 
sufficiently  to  amount  to  a  considerable  dilatation,  which  had 
caused  some  pressure  on  the  great  veins,  hence  the  congestion  of 
the  base  of  the  neck,  and  the  prominence  of  the  innominate  artery. 

It  was  now  easy  to  understand  the  frequency  and  intensity  of 
her  angina.  The  heart-muscle  simply  could  not  be  flushed  with 
blood  through  the  extremely  narrowed  coronary  ostia.  Whenever 
physical  exertion  called  for  more  1)1o(k1  witliiu  the  coronary  arter- 


AORTIC  REGURGITATION  295 

ies  it  was  hot  forthcoming,  and  cardiac  ischsemia  was  manifested 
by  a  cry  of  agony. 

From  the  foregoing,  it  is  plain  that  cases  of  aortic  regurgita- 
tion can  be  divided  into  two  classes.  In  the  one,  the  lesion  is  the 
result  of  endocarditis,  contracted  during  a  period  of  life  when  the 
myocardium  and  arterial  walls  are  still  young  and  healthy — great 
compensatory  hypertrophy  is  possible,  and  the  disease  may  endure 
for  many  years  without  giving  rise  to  symptoms.  These  appear  at 
length  only  after  the  heart-muscle  can  no  longer  be  sustained  by 
the  coronary  circulation,  or  the  breakdown  occurs  as  the  result  of 
fresh  endocarditis  ingrafted  on  the  old  process  in  the  course  of 
acute  articular  rheumatism.  In  my  care,  five  years  ago,  was  a  viva- 
cious young  lady  of  eighteen,  who  presented  the  typical  signs  of 
free  aortic  regurgitation,  a  quick,  collapsing  pulse,  a  broad,  heav- 
ing apex-beat.,  situated  far  below  and  to  the  left  of  its  normal 
situation,  and  a  loud  diastolic  murmur.  She  consulted  me  because 
of  having  noticed  that  she  could  no  longer  run  upstairs,  dance, 
ride  a  wheel,  or  do  other  things  which  before  were  unattended 
with  consciousness  of  the  heart's  action.  She  did  not  get  out  of 
breath,  but  was  annoyed  by  forcible  pounding  of  the  heart  and  by 
the  occasional  sensation  as  if  it  "  gave  a  flop." 

She  had  some  flatulent  indigestion  and  was  constipated.  The 
pulse  was  now  and  then  intermittent,  and  for  the  purpose  of  cor- 
recting this  intermittence  she  was  given  small  doses  of  tincture 
of  digitalis,  5  drops  3  times  a  day.  When  she  next  returned,  after 
a  few  days,  she  stated  that  the  pounding  of  the  heart  was  worse 
instead  of  better.  The  digitalis  was  reduced,  but  still  intensified 
her  symptoms,  and  was  discontinued.  Thinking  that  the  inter- 
missions might  be  due  to  gastro-intestinal  derangement,  she  was 
given  remedies  to  correct  the  constipation  and  improve  digestion. 
There  was  some  improvement,  but  still  the  heart  did  not  become 
entirely  regular.  One  day  she  complained  of  dull  frontal  head- 
ache, some  pains  and  stiffness  of  the  muscles,  which  seemed  to  me 
a  muscular  rheumatism,  possibly  of  uric-acid  origin.  Accord- 
ingly, she  was  put  upon  potash  and  salicylate  of  soda,  and  or- 
dered to  drink  freely  of  water.  This  was  a  happy  hit,  for  she 
lost  the  intermittence  of  the  pulse,  and  was  no  longer  annoyed  by 
the  heart's  pounding. 

A  year  later,  believing  I  had  discovered  evidence  of  a  tendency 


296  DISEASES  OF  THE  HEART 

to  growing  dilatation  of  the  left  ventricle,  I  gave  her  a  course  of 
]Sraulieini  baths,  which  agreed  with  her,  and  she  felt  so  well  that 
I  lost  track  of  her  for  some  months.  Indeed,  with  one  exception, 
after  the  baths  were  finished,  I  never  saw  her  again.  But  one 
day,  encountering  her  mother  in  the  cars,  I  learned  that  in  Au- 
gust, eight  months  subsequent  to  her  last  visit  at  mj  office,  she 
developed  what  appeared  to  be  a  mild  attack  of  articular  rheu- 
matism. As  I  was  out  of  the  city,  a  neighbouring  physician  was 
given  charge  of  the  case,  and  he  very  properly  confined  her  to 
bed.  After  about  a  week  the  rheumatic  manifestations  had  sub- 
sided, and  she  was  thought  to  be  getting  on  finely.  One  morn- 
ing she  awoke  in  excellent  spirits  and  seemed  nowise  in  imme- 
diate danger.  Nevertheless,  during  the  forenoon,  when  she  sat 
up  in  bed  to  drink  a  glass  of  water,  she  suddenly,  without  warn- 
ing, fell  back  upon  her  pillow  and  expired.  No  autopsy  was  held, 
and  I  have  no  means  of  knowing  the  exact  condition,  but  I  be- 
lieve that  probably  the  heart  had  become  weakened  by  fresh  endo- 
carditis attending  the  mild  rheumatic  attack,  and  under  such  cir- 
cumstances the  exertion  of  sitting  up  occasioned  sudden  diastolic 
arrest  of  the  left  ventricle.  It  simply  illustrates  the  liability  of 
these  patients  to  sudden,  unexpected  death. 

In  the  second  class  belong  patients  whose  valvular  defect  is 
the  local  manifestation  of  degenerative  changes,  which,  if  not  due 
to  syphilis,  the  gouty  diathesis,  strain,  and  the  like,  are  associated 
with  advancing  age.  In  such  persons  compensatory  hypertrophy 
rarely  proves  so  enduring  as  in  the  young,  and  may  fail  early, 
because  the  myocardium  is  already  degenerated,  or  because  the 
state  of  the  coronary  arteries  does  not  permit  that  degree  of  nour- 
ishment necessary  to  the  maintenance  of  hypertrophy.  In  this 
second  class  should  also  be  reckoned  those  cases  in  which  the  aortic 
insufficiency  is  the  result  of  rupture.  In  this  latter  group,  pain, 
praecordial  distress,  and  other  symptoms  of  cardiac  incompetence 
are  apt  to  appear  promptly  after  the  injury,  and  to  persist  without 
relief.  Naturally,  however,  the  ability  of  the  heart  to  compensate 
the  defect  depends  upon  the  extent  of  rupture — that  is,  the  degree 
of  regurgitation  jx'nn itted — and  ii]xin  the  state  of  the  heart-mus- 
cle. Dilatation  of  the  left  ventricle  usually  develops  rapidly,  with 
little  or  no  hypertrophy,  and  hence  after  a  few  weeks  or  months 
the  heart  succumbs. 


AORTIC  REGURGITATION  297 

In  persons  suffering  from  slowly  induced  degenerative 
•changes  symptoms  appear  slowly,  but  are  never  so  delayed  in  com- 
ing as  in  patients  whose  incompetence  originate  in  endocarditis. 
In  most  instances  the  symptoms  that  initiate  breaking  compen- 
sation are  such  as  may  be  referred  either  to  cerebral  anaemia — 
i.  e.,  vertigo  and  syncopal  attacks — or  to  cardiac  fatigue  and  de- 
generation— i.  e.,  irregularities  of  the  pulse,  palpitation,  and 
angina  pectoris. 

When,  on  the  other  hand,  cardiac  failure  leads  to  stasis  in  the 
lesser  circulation,  or  in  the  great  veins  of  the  general  system^  the 
symi^toms  gradually  become  those  of  the  terminal  stage  of  mitral 
disease — i.  e.,  dyspnoea,  cough,  and  frothy,  or  it  may  be  sati- 
guineous  expectoration,  disturbed  visceral  functions  in  general, 
■oedema,  and  attacks  of  threatening  asystolism.  When  at  last  aortic 
regurgitation  has  reached  this  stage  the  struggle  is  less  likely  to 
be  protracted,  and  death  is  usually  more  sudden  than  in  defects  at 
the  left  auriculo-ventricular  orifice. 

Physical  Signs. — Inspection. — In  cases  of  pronounced 
■aortic  regurgitation  the  disease  reveals  its  presence  to  the  skilled 
eye  by  the  throbbing  of  the  temporal  and  carotid  arteries.  In 
contrast  with  the  cyanosis  of  mitral  disease  the  aspect  of  the  pa- 
tient is  apt  to  present  more  or  less  pallor,  especially  if  the  disease 
has  developed  in  early  life.  Inspection  of  the  chest  usually  de- 
tects strong  pulsation  of  the  cardiac  area  to  the  left  of  the  ster- 
num, the  degree  and  extent  of  this  pulsation  depending  upon  the 
thinness  and  flexibility  of  the  chest-wall,  as  well  as  on  the  hyper- 
trophy of  the  heart.  Occasionally  a  wave-like  impulse  is  seen  to 
pass  from  the  base  downward  towards  the  apex-beat,  while  in 
some  cases  there  may  be  slight  systolic  retraction  of  the  third 
and  fourth  interspaces  to  the  left  of  the  sternum,  in  consequence 
of  atmospheric  pressure,  as  the  hypertrophied  heart  recedes  from 
the  chest-wall. 

The  apex-beat  is  displaced  outward  and  downward,  in  some 
■cases  even  as  far  as  the  seventh  or  eighth  left  intercostal  space, 
close  to  the  left  anterior  axillary  line.  It  is  broad  and  heaving, 
at  once  conveying  the  impression  of  a  large  and  powerful  organ. 
In  the  young,  with  broad  intercostal  spaces,  the  dimensions  of  the 
left  ventricle  may  be  almost  as  accurately  delineated  by  the  vis- 
ible impulse  as  by  percussion. 
21 


298  DISEASES  OF  THE  HEART 

In  niicklle-aged  individuals,  on  the  contrary,  particularly  if 
the  chest  is  capacious,  the  apex-beat  may  be  scarcely  perceptible. 
In  some  instances,  no  doubt,  this  is  owing  to  the  inability  of  the 
degenerated,  heart  to  establish  great  compensatory  hypertrophy. 
When  very  free  regurgitation  is  compensated  by  great  hyper- 
trophy, the  eye  sometimes  discerns  visible  pulsation  in  the  periph- 
eral arteries,  as  the  radial  or  the  dorsalis  pedis.  This  phenom- 
enon, which  is  brought  out  with  special  distinctness  by  extension 
of  the  hand  or  foot,  is  the  ocular  manifestation  of  that  peculiar- 
ity of  the  pulse  about  to  be  described  under  palpation  as  the  pulsus 
altus  et  celer. 

Quincke  has  described  a  visible  pulsation  of  the  retinal 
artery,  which  may  be  more  or  less  tortuous  and  elongated  with 
each  pulsation.  Capillary  and  venous  pulse  will  be  considered 
later  on. 

Palpation. — The  hand  laid  upon  the  praccordium  detects  pow- 
erful cardiac  impulse,  and  over  the  apex-beat  sometimes  perceives 
a  short  presystolic  thrill,  or  rather  receives  an  impression  as  if 
the  tip  of  the  heart  slid  up  to  its  maximum  impulse.  The  impact 
of  the  apex  resembles  the  striking  of  a  huge  fist  against  the  chest- 
wall,  and  if  the  patient  be  slight,  the  whole  chest  may  seem  to 
quiver  with  the  shock.  Systolic  thrill  is  sometimes  felt  in  the 
aortic  area.  Under  some  circumstances  a  diastolic  thrill  is  also 
manifest. 

The  most  remarkable  feature  in  this  part  of  the  examination 
is  presented  by  the  pulse.  Its  characteristics  are  so  distinctive  that 
a  diagnosis  is  often  possible  from  it  alone.  First  carefully  stud- 
ied and  accurately  described  by  Sir  Dominick  Corrigan,  it  is  often 
called  Corrigan  pulse,  while  other  terms  applied  to  it  are  the 
collapsing  pulse,  the  water-hammer  pulse,  the  locomotive  pulse^ 
and  the  pulsus  alius  et  celer.  In  well-marked  cases  the  finger 
laid  upon  the  radial  artery,  or  upon  any  other  readily  accessible 
artery  for  that  matter,  is  suddenly  lifted  by  a  large,  powerful 
pulse-wave,  which,  advancing  swiftly  along  the  vessel,  strikes  the 
finger  like  a  shot  or  ball,  and  then  instantly  recedes.  The  vessel, 
in  other  words,  after  Ix-iiig  (piickly  distended  as  quickly  collapses, 
hence  the  name  colla])siiig  pulse.  It  is  well  shown  in  the  accom- 
panying tracing  (Fig.  54). 

This  characteristic  of  the  pulse  is  intensified  by  raising  the 


AORTIC   REGURGITATION  299 

jDatient's  hand  to  a  level  higher  than  that  of  the  heart,  and  thus 
allowing  the  force  of  gravity  to  hasten  the  quick  recession  of  the 
pulse-wave. 

The  quickness  of  the  pulse-wave  has  thus  been  dwelt  upon  for 
the  purpose  of  emphasizing  the  difference  between  the  speed  with 
which  it  travels  along  the  artery,  and  the  frequency  with  which 


Fig.  54. — Sphygmogram  of  Aoetic  Eegurgitation. 
Tracing  by  Dr.  Edward  F.  Wells. 

the  individual  pulse-waves  follow  each  other.  Consequently,  a 
frequent  pulse  is  a  rapid  or  accelerated  pulse,  whereas  a  quick 
pulse  is  one  that  strikes  the  finger  suddenly  and  is  not  sustained. 
A  pulse  may  be  both  frequent  and  quick,  as  in  fever,  but  a  quick 
pulse  does  not  necessarily  have  to  be  also  a  rapid  one.  In  aortic 
regurgitation,  however,  the  pulse  is  both  sudden  and  accelerated. 

In  some  cases  when  the  arteries  have  become  more  or  less 
sclerotic  and  tortuoiTS  the  bounding  pulse-wave ,  seems  to  lift  the 
vessel  from  its  bed,  and  hence  some  writers  have  spoken  of  it  as 
the  locomotive  pulse.  To  make  the  raison  d'etre  of  this  collaps- 
ing character  understood,  it  is  necessary  to  describe  how  the  valvu- 
lar disease  under  consideration  modifies  pulse-tension. 

Under  normal  conditions  blood-pressure  within  the  arterial 
system  is  maintained  at  a  uniform  height  by  the  periodic  dis- 
charge of  blood  into  the  aorta  and  by  the  elastic  recoil  of  the 
arterial  walls  aided  by  the  tightly  closed  semilunar  valves.  The 
blood-stream  driven  against  the  valve  by  the  recoiling  aortic  walls 
is  intercepted  and  forced  onward  through  the  arterial  system.  If 
the  aortic  valves,  incompetent  by  disease,  are  unable  to  check  the 
backward  flow  of  the  blood  a  portion  of  it  regurgitates  into  the 
left  ventricle,  and  blood-pressure  in  the  arterial  system  is  corre- 
spondingly lowered  instead  of  being  maintained  at  a  uniform 
level.  Accordingly,  the  Avave  of  blood  constituting  the  pulse- 
wave  quickly  recedes  and  allows  the  arterial  walls  to  collapse,  as 
it  were.    .The  hypertrophied  left  ventricle,  made  more  than  nor- 


300  DISEASES   OF   THE   HEART 

nially  capacious  by  dilatation,  discharges  its  contents  with  a  de- 
gree of  energy  proportionate  to  its  hypertrophy;  and  as  its  con- 
tents are  angmented  oyer  the  normal  by  the  amount  that  has  the 
moment  before  regurgitated,  the  aorta  becomes  powerfully  dis- 
tended by  this  abnormally  large  mass  of  blood.  In  consequence 
of  the  partial  emptiness  of  the  arteries  caused  by  the  regurgita- 
tion the  large  blood-waye  meets  with  but  little  resistance,  and 
trayelling  rapidly  towards  the  periphery,  distends  the  arteries  in 
its  course. 

Hence  the  greater  the  compensatory  hypertrophy  of  the  left 
ventricle,  the  fuller,  stronger,  and  quicker  will  be  the  pulse.  The 
freer  the  regurgitation  the  more  marked  will  be  the  collapse  of 
the  yessel-walls.  The  degree  of  difference,  therefore,  between  the 
distention  and  collapse  of  the  artery  is  a  measure  not  only  of  the 
degree  of  the  regurgitation,  but  also  of  the  resulting  compensatory 
hypertrophy,  for  when  the  left  yentricle  begins  to  fail,  this  pecul- 
iar collapsing  quality  of  the  pulse  grows  less  pronounced,  although 
the  regurgitation  is  no  whit  less  free. 

Very  exceptionally  the  pulse  is  said  to  exhibit  the  character 
knoAvn  as  bisferiens  and  represented  in  Fig.  55.     If  the  finger  is 

pressed  lightly  on  the  artery 
it  receiyes  a  sensation  as  if 


the  pulse-waye  were  divided 
into   two   portions,   of  which 
Fig.  55.— p.  bisferiens.  the    sccoud    is    the    Stronger. 

Allbutt's  Syst.  of  Med.,  vol.  V,  p.9.31.  rT^^  ^  , 

1  he  lormor  represents  the 
sudden  distention  of  the  artery,  and  the  latter  is  the  palpable  ex- 
pression of  the  pra-dicrotic  or  tidal  wave.  Pulsus  bisferiens  is  usu- 
ally stated  to  be  found  in  aortic  obstruction,  but  according  to 
Graham  Stecll,  cited  by  Clifford  Allbutt,  undoubtedly  occurs  in 
some  cases  of  regurgitation  associated  with  little  if  any  stenosis. 
In  one  of  Steell's  instances  this  peculiarity  was  not  equally  con- 
stant or  pronounced  on  both  sides  of  the  body.  Its  production  is 
therefore  difficult  of  explanation,  as  well  as  inconstant.  I  have 
never  obtained  a  tracing  showing  a  bisferiens  pulse  in  aortic  insuf- 
ficiency, but  T  have  certainly  felt  pulses  in  some  cases  which,  to  my 
finger,  seemed  plainly  of  this  character. 

Not  infrequently,  pulsation  is  so  pronounced  in  the  arterioles 
that  the  fingers  of  the  patient  throb  appreciably  when  grasped 


AORTIC   REGURGITATION  301 

and  the  diagnosis  of  his  malady  can  be  made  while  in  the  act  of 
shaking  his  hand. 

Two  other  phenomena,  the  capillary  pulse  and  visible  venous 
pulse,  should  properly  have  been  described  under  inspection,  but 
have  been  reserved  until  now  for  the  reason  that  they  will  be  bet- 
ter understood  after  what  has  just  been  said  concerning  the  pecu- 
liarities of  the  pulse.  In  cases  in  which  arterial  tension  is  very 
low  in  consequence  of  free  regurgitation,  the  capillaries  are  dis- 
tended by  the  blood-wave  instead  of  being  kept  uniformly  filled, 
and  hence  display  what  is  known  as  the  capillary  pulse  (Quincke's 
sign).  This  may  be  well  seen  in  the  palm  and  beneath  the  nails 
when  the  hand  is  warm,  or  it  may  be  evoked  by  friction  of  the 
skin — e.  g.,  of  the  forehead — until  an  area  of  hypersemia  is  pro- 
duced. If  the  periphery  of  such  a  red  zone  is  closely  watched,  its 
edge  will  be  seen  to  alternately  advance  with  each  systole  and 
recede  with  each  diastole  of  the  heart.  Capillary  pulsation  is  also 
sometimes  plainly  visible  on  the  soft  palate. 

By  venous  pulse  is,  meant  a  visible  pulsation  in  the  superficial 
veins.  This  is  sometimes  well  marked  in  the  subcutaneous  veins  of 
the  back  of  the  hand  and  the  forearm  when  the  extremity  is  al- 
lowed to  hang  down  until  the  vessels  become  turgid.  This  venous 
pulse  is  a  slow  undulatory  wave  which,  as  Broadbent  suggests,  may 
be  best  noticed  by  laying  a  filament  of  sealing  wax  across  the  sur- 
face of  the  vein.  Venous  pulsation  is  specially  pronounced  when 
arterial  tension  has  been  still  further  reduced  by  fever.  Neither 
of  these  last  two  phenomena  is  peculiar  to  aortic  regurgitation,  for 
they  may  be  observed  in  severe  anaemia  which  has  sufficiently 
lowered  pulse-tension.  They  are,  however,  most  distinct  and  typ- 
ical in  aortic  incompetence. 

Finally,  when  regurgitation  is  very  free,  a  distinct  thrill  may 
be  felt  in  the  cervical  arteries  and  even  in  the  brachials.  This  was 
well  felt  in  a  man  of  about  thirty-five,  who  died  suddenly  a  few 
weeks  subsequently.  In  this  case  the  thrill  was  palpable  when 
the  finger  was  laid  ever  so  lightly  on  the  vessel,  and  seemed  to  bo 
but  the  palpable  expression  of  vibrations  imparted  to  the  arterial 
coats  by  the  suddenness  and  violence  of  the  impact  of  the  blood- 
stream. 

Percussion. — As  in  other  cases  of  valvular  disease,  percussion 
affords  our  best  means  of  noting  to  what  extent  and  in  what  direc- 


302 


DISEASES   OF   THE   HEART 


tion  the  heart  has  suffered  enlargement.     It  is  particularly  valu- 
able in  cases  in  which  the  size  of  the  chest  or  the  feebleness  of 

cardiac  impulse  prevents  us 
from  judging-  of  the  size  of 
the  heart  by  inspection  and 
palpation.  In  compensated 
cases  cardiac  dulness  is  in- 
creased only  to  the  left  and 
downward,  and  the  outline 
of  the  left  ventricle  is  rather 
pointed  (Fig.  56).  As  dila- 
tation comes  on,  the  left  car- 
diac border  becomes  more 
rounded  and  the  apex  is  blunt 
and  broad,  so  that  one  should 
always  strive  to  percuss  out 
the  shape  of  the  left  ventricle 


Fiii.  i)ii. — T vfE  uF  KtLATivi.  Dllness  in  Well- 
compensated  Aortic  Eegi'rgitation. 


from 

57). 

and  is 

es   de- 


as   well   as    its   distance 
the    median    line    (Fig. 
Increased  dulness  to  the  right  is  present  only  secondarily, 
a  measure  of  back  pressure  important  to  determine. 

Auscultation. — Regurgitation  through  the  aortic  valv 
clares  itself  by  a  murmur  syn- 
chronous with  the  second 
heart  sound  and  therefore 
diastolic  in  time,  which  is 
heard  with  greatest  intensity 
over  the  l^ase  of  the  heart  any- 
where between  the  second 
right  costo-sternal  articulation 
and  the  junction  of  the  fifth 
left  costal  cartilage  with  the 
l)reastbone  (Figs.  58  and  59). 
Its  most  usual  scat  of  maxi- 
mum loudness  is  on  the  body 
of  the  sternum  at  the  level  o1 
the  third  costal  cartilage,  and 

.     •  •       .  •.  Fkj.    57. — Tvi'i'.    UK    Relative    Dulnems    in 

vet  in  some  instances  it  mav  ;.  . 

'-  •  I'ooKLV  (.  omi'ensatei)  Aoutio   Kequiwi- 

be  heard  most  j  da  inly  or  heard  tation. 


AORTIC  REGURGITATION 


503 


only  in  the  fourth  left  interspace,  close  to  the  breastbone.  It  is 
generally  most  distinct  in  the  erect  position  or  when  the  heart's 
action  is  excited.  ISTeverthe- 
less  I  have  certainly  observed 
cases  in  which  the  murmur  be- 
came more  distinct  and  easily 
recognised  when  the  patient 
was  recumbent.  This  murmur 
is  transmitted  downward  to- 
wards the  ensiform  appendix, 
and  in  some  instances  also 
towards  the  left,  even  as  far 
as  the  apex.  When  audible, 
with  more  than  usual  inten- 
sity at  the  apex,  the  murmur 
is  thought  by  some  to  indicate 
incompetence  of  the  left  pos- 
terior flap. 

As     previously     remarked 
with   reference   to   the   mitral 
reffurgitant  murmur,  the  intensitv  and  the  extent  of  conduction  of 
this  aortic  diastolic  murmur  furnish  no  criterion  of  the  gravity  of 


Fia.  58. — Spot  of  Maximum  Intensity 
(small  ciecle)  and  Area  of  Transmis- 
sion OF  Typical  Aortic  Keglrgitant 
Murmur. 


Fig.  59. — Khythm  of  Aortic  Regurgitant  Murmur. 

the  lesion.     Indeed,  numerous  instances  have  been  recorded  in 
which  no  bruit  at  all  was  audible  for  a  variable  time  immediately 


304  DISEASES  OP  THE   HEART 

prior  to  death.  This  is  probably  owing  to  a  want  of  sufficient 
force  and  rapidity  in  the  regurgitant  stream  to  generate  sonifer- 
ous vibrations.  The  duration  of  this  murmur  is  usually  short,  and 
its  quality  is  soft  rather  than  harsh,  and  is  unlike  that  of  any 
other  murmur  excepting  the  bruit  of  pulmonary  regurgitation. 

In  exceptional  cases  the  diastolic  aortic  murmur  may  have  a 
true  musical  tone.  I  Avell  recall  the  case  of  a  coloured  man,  in 
whom  the  intra-vitam  diagnosis  of  aortic  regurgitation  was  sub- 
stantiated post  mortem,  and  who  presented  this  musical  quality 
in  a  most  marked  degree,  but  not  with  every  ventricular  diastole. 
At  irregular  intervals  the  soft  diastolic  bruit  was  associated  with^ 
or  replaced  by  a  musical  murmur  so  intense  that  it  was  heard  by 
the  patient,  and  imparted  a  distinct  thrill  to  the  hand  laid  upon 
the  heart  to  the  left  of  the  sternum.  A  few  days  before  death 
this  musical  murmur  entirely  subsided,  and  at  the  post-mortem 
examination  no  condition  that  could  explain  its  production  could 
be  discovered,  although  diligently  sought  for.  The  valves  pre- 
sented the  appearance  ordinarily  found  in  cases  of  endocarditic 
insufficiency. 

The  heart-sounds  usually  present  more  or  less  modification. 
The  first  sound  at  the  apex  is  apt  to  be  mufiled  or  toneless,  while 
the  second  sound  is  enfeebled.  In  the  aortic  area  the  second 
sound  may  be  entirely  wanting,  being  replaced  by  the  diastolic 
murmur,  or  there  may  be  a  faint  rudimentary  second  sound.  The 
aortic  first  sound  may  be  audible  or  replaced  by  a  rough,  more  or 
less  intense,  systolic  murmur.  This  bruit  is  usually  interpreted 
as  signifying  an  associated  stenosis.  This  conclusion,  however,  is 
not  always  justifiable,  since  such  a  systolic  murmur  may  be  due 
either  to  roughness  without  narrowing  of  the  orifice,  or  to  sclero- 
sis of  the  aortic  intima.  When  both  a  systolic  and  diastolic  mur- 
mur are  heard,  they  are  often  spoken  of  as  a  "  to  and  fro  "  mur- 
mur, and  such  a  combination  is  very  frequent. 

There  are  also  certain  auscultatory  phenomena  connected  with 
the  peripheral  arteries  which  furnish  valuable  secondary  signs  of 
this  valvular  lesion.  Over  the  carotid  and  subclavian  arteries  a 
faint  systolic  murmur  is  often  found  to  replace  the  first  sound, 
while  if  the  regurgitation  is  free  the  normal  second  tone  is  ab- 
sent. When  one  auscultates  the  fomorals,  he  hears  a  sharp  snap, 
which  is  synchronous  with  ventricular  systole  and  is  the  audible 


AORTIC  REGURGITATION  305 

expression  of  the  sudden  tension  into  which  the  arterial  coats  are 
thrown  as  they  are  distended  by  the  large  sudden  pulse-wave.  If 
rather  more  pressure  is  exerted  upon  the  vessel  by  means  of  the 
stethoscope,  this  snapping  tone  disappears  and  becomes  replaced 
by  a  distinct  murmur,  the  murmur  of  constriction,  which  can  be 
elicited  over  any  artery  of  sufficient  size  when  no  valvular  disease 
exists.  When  regurgitation  is  free,  it  is  usually  possible  by  trying 
different  degrees  of  pressure  to  at  length  bring  out  more  or  less 
clearly  not  only  this  systolic  murmur,  but  also  a  diastolic  one,  so 
that  one  becomes  conscious  of  a  double  murmur,  of  which,  in  my 
experience,  the  systolic  is  usually  the  louder.  This  double  femoral 
bruit  was  first  described  by  Duroziez,  and  hence  is  often  spoken 
of  as  Duroziez's  sign.  It  is  considered  pathognomonic  of  aortic 
regurgitation,  since  in  no  other  disease  are  the  conditions  pre- 
sented for  its  production.  The  explanation  of  this  phenomenon 
is  as  follows: 

Constriction  of  the  artery  throws  the  blood-stream  into  audi- 
ble vibrations  as  it  passes  the  point  of  pressure,  and,  normally,  this 
is  all;  but  in  aortic  insufficiency  the  blood-wave  recedes  during 
diastole  and  passes  again  this  point  of  constriction,  with  the  result 
that  it  is  a  second  time  thrown  into  vibrations,  and  a  diastolic 
murmur  is  generated.  In  most  cases  these  acoustic  phenomena 
are  elicited  only  over  arteries  of  large  calibre,  but  when  the  lesion 
is  very  pronounced  and  the  left  ventricle  is  powerful,  both  the  sys- 
tolic snap  and  the  double  bruit  may  be  heard  in  small  vessels,  as 
the  radial  and  even  the  dorsalis  pedis. 

Diagnosis. — Ordinarily  the  recognition  of  aortic  insufficiency 
is  not  difficult.  In  some  instances  it  may  be  detected  at  a  glance, 
but  when  the  individual  is  past  middle  age,  with  sclerotic  arteries 
and  a  voluminous  thorax,  the  collapsing  character  of  the  pulse 
and  a  powerful  cardiac  impulse  may  not  be  pronounced,  and  care 
is  requisite  to  determine  that  the  condition  is  not  an  aortic  aneu- 
rysm that  has  led  to  regurgitation.  In  all  doubtful  or  indistinct 
cases  particular  study  should  be  given  to  the  vascular  signs,  since 
they  are  conclusive,  and  a  diastolic  bruit  is  not.  Indeed  it  is  to 
be  remembered  that  when  in  the  last  stages  the  heart  has  become 
very  weak,  the  murmur  previously  present  may  entirely  disappear. 
Moreover,  the  diagnosis  of  this  lesion  may  be  rendered  not  easy  by 
the  association  of  relative  mitral  incompetence,  or  of  other  organic 


306  DISEASES  OF  THE   HEART 

defects.  In  all  such  cases  one  must  minutely  investigate  the  vas- 
cular system  and  rely  on  its  disclosures  rather  than  on  cardiac 
findings,  although  even  here  valuable  information  may  be  obtained 
if  attention  is  paid  to  the  secondary  changes  instead  of  the  auscul^ 
tatory  findings. 

Before  leaving  the  subject  of  the  diagnosis  of  this  disease,  I 
desire  to  dwell  for  a  few  moments  on  a  subject  which  has  given 
rise  to  much  controversy.  Many  years  ago  the  late  Austin  Flint, 
one  of  the  most  careful  clinical  observers  this  country  has  pro- 
duced, directed  attention  to  tho  presence  of  a  presystolic  apex- 
murmur  in  some  cases  of  aortic  regurgitation,  and  declared  it  was 
an  accidental  murmur  which  did  not  necessarily  denote  the  co- 
existence of  mitral  stenosis.  He  was  vehemently  attacked  by  Bal- 
four, who  declared  a  functional  presystolic  murmur  an  impossi- 
bility. But  corroboration  of  Flint's  ol)servation  has  come  from 
so  many  sources  that  there  can  no  longer  be  any  doubt  of  the  cor- 
rectness of  his  statements. 

His  explanation  of  the  mode  of  its  production  is,  however, 
probably  not  correct  in  the  light  of  more  recent  physiological 
knowledge  concerning  the  closure  of  the  mitral  valves.  The  mur- 
mur is  now  thought  due  to  vibrations  of  the  mitral  curtains  as  they 
are  caught  between  the  regurgitant  stream  on  the  one  hand,  and 
that  pouring  out  of  the  left  auricle  on  the  other.  It  is  quite  pos- 
sible for  mitral  constriction  and  aortic  regurgitation  to  coexist, 
and  in  any  instance  of  this  latter  disease  in  which  a  mitral  presys- 
tolic murmur  is  recognised  its  correct  interpretation  is  made  pos- 
sible by  giving  due  consideration  to  the  presence  or  absence  of 
secondary  changes  in  the  right  ventricle,  and  the  smallness  yet 
colljijising  cliaracter  of  the  radial  pulse. 

Prognosis. — A  proper  estimation  of  the  prognosis  of  aortic 
regurgitation  requires  a  sharp  distinction  between  the  forms  due 
to  endocarditis  and  those  of  degenerative  origin.  Furthermore, 
in  each  group  and  in  each  individual  instance,  the  jM'ognosis  is  in 
direct  relation  to  the  degree  of  compensatory  hypertrophy,  the 
same  as  in  any  other  valvular  defect.  If,  in  the  first  class — that 
is,  of  endocarditic  origin — compensation  becomes  once  well  estab- 
lished, it  is  possible  for  the  disease  to  be  borne  for  many  years. 
Mr.  W.,  the  description  of  whose  sudden  death  will  be  narrated, 
was  known  to  have  aortic  regurgitation  of  severe  type  for  at  least 


AORTIC  REGURGITATION  307 

twenty-eight  years,  and  perhaps  longer.  When,  however,  com- 
pensation begins  to  fail,  the  prognosis  is  very  grave,  for  it  cannot 
be  so  readily  restored  as  in  mitral  disease.  Indeed,  some  authors 
are  of  the  oj)inion  that  compensation  can  never  be  reinstated;  at 
the  most  there  being  hope  only  of  retarding  the  downward 
progress. 

When  in  the  second  category  of  cases,  those  of  degenerative 
nature,  compensation  becomes  established,  it  is  at  the  best  only  for 
a  comparatively  limited  period,  owing  to  the  probable  presence  of 
chronic  myocarditis,  and  when  this  compensation  once  breaks,  it 
is  irretrievably  gone.  Henceforth  the  progress  of  the  malady  is 
for  the  most  part  steadily  downward.  In  all  cases  the  prospect  of 
even  partial  recovery  is  slight,  and  of  restoration  to  a  life  of  ac- 
tivity and  freedom  from  symptoms  is  nil. 

It  is  stated  that  very  rarely  a  regurgitation  may  be  converted 
into  a  predominating  stenosis  by  the  growth  on  the  valves  and 
ring  of  vegetations,  in  consequence  of  fresh  endocarditis;  and 
whenever  this  occurs  the  prognosis  becomes  more  favourable,  pro- 
vided, of  course,  there  be  no  myocarditis  or  other  complications. 
This  possibility  is  too  remote  to  be  ordinarily  taken  into  considera- 
tion. 

Mode  and  Causes  of  Death. — ISTo  other  valvular  disease 
so  often  terminates  abruptly.  The  suddenness  of  the  death  is  due 
to  paralysis  of  the  left  ventricle  in  diastole.  In  most  cases,  no 
doubt,  warning  has  been  given  of  the  pending  catastrophe  by  ir- 
regularities of  the  pulse,  vertigo,  or  other  symptoms  which  failed 
at  the  time  to  attract  the  patient's  attention,  or  were  too  insig- 
nificant to  impress  him  with  their  gravity.  Death  follows  some 
sudden  effort,  as  assuming  the  erect  from  the  recumbent  position, 
springing  out  of  a  chair  to  leave  the  room,  jumping  on  to  a  moving 
street-car,  and  the  like.  The  muscular  effort  incident  to  such  sud- 
den movements  abruptly  raises  blood-pressure  within  the  vessels 
supplying  the  groups  of  contracted  muscles,  and  drives  the  blood 
into  the  left  ventricle  during  its  period  of  relaxation  with  a  degree 
of  force  which  the  ventricle  is  unable  to  resist.  It  fails  to  respond 
by  a  subsequent  systole,  and  the  patient  falls  to  the  ground  in  an 
attack  of  fatal  syncope. 

Fortunately  for  the  patient,  as  well  as  for  the  peace  of  mind 
of  his  friends,  assurance  can  be  given  that  sudden  death  in  the  way 


308  DISEASES  OF  THE  HEART 

just  described  is  not  usual.  Indeed,  it  occurs  in  the  minority  of 
cases  of  aortic  regurgitation.  According  to  Broadbent,  it  occurred 
in  10  out  of  38  cases  taken  from  the  records  of  St.  Mary's  Hos- 
pital. Sudden  death  occurs  by  far  the  most  frequently  as  result 
of  fibroid  and  fatty  degeneration  of  the  myocardium,  and,  there- 
fore, we  should  look  for  it  in  individuals  whose  aortic  valves  are 
incompetent  in  consequence  of  degenerative  changes  rather  than 
in  the  young,  whose  valvular  lesion  is  of  endocarditic  origin.  This 
does  not  apply,  however,  when  the  heart  is  freshly  attacked  by  an 
acute  endocarditis.  The  case  of  the  young  lady  of  eighteen  illus- 
trates that  under  such  circumstances  the  end  may  come  unex- 
pectedly and  without  warning. 

We  have  seen  in  most  cases  of  aortic  regurgitation  that  the 
symptoms  showing  complete  loss  of  compensation  become  those  of 
pronounced  venous  stasis,  the  same  as  in  the  last  stage  of  mitral 
disease.  It  is  to  be  expected,  therefore,  that  exitus  lethalis  should 
take  place  in  the  same  manner,  and  in  fact  such  is  the  case — i.  e., 
from  gradual  cardiac  asthenia  or  acute  pulmonary  oedema. 

Striimpell  directs  attention  to  the  not  infrequent  occurrence 
of  pericarditis  in  aortic  insufficiency,  particularly  when  the  valves 
have  been  attacked  by  fresh  inflammation,  and  in  such  the  peri- 
carditis is  very  apt  to  lead  to  the  death  of  the  patient. 

Of  24  cases  analyzed  by  Hustedt,  the  causes  of  death  were  as 
follows :  Heart-weakness,  8  ;  pulmonary  infarct,  9  ;  pneumonia,  2  ; 
oedema  of  the  lungs,  3 ;  apoplexy,  1 ;  and  pleuritis,  1. 

The  suddenness  of  death  is  illustrated  by  the  case  of  ^fr.  W., 
aged  forty-five,  who  had  had  aortic  insufliciency  dating  from 
chorea  and  rheumatism  in  boyhood,  and  had  shown  symptoms  of 
failing  compensation  for  at  least  two  years.  These  consisted  in 
feebleness  and  irregularity  of  the  pulse,  and  attacks  of  weakness 
and  faintness  of  such  severity  that  they  compelled  him  to  seek  aid 
of  the  nearest  physician,  Notwithstanding  the  extreme  degree 
of  fatigue  and  exhaustion  occasioned  by  his  duties,  he  persisted  in 
the  daily  attendance  at  his  oflice.  The  day  of  his  death  he  left 
home  as  usual  and  proceeded  to  his  place  of  business.  While  in 
the  act  of  stooping  over  a  table,  he  sank  to  the  floor,  and  ex- 
flaimed,  "  I  am  dying!  "  His  clerk,  who  was  standing  near,  lifted 
him  into  a  chair,  and  asked  if  he  should  run  for  a  doctor.  The 
sufl'erer  looked  up,  smiled,  and  shook  his  head,  as  much  as  to  say, 


AORTIC  REGURGITATION  309 

*^  No,  it  is  of  no  use,"  and  a  few  moments  thereafter  he  quietly 
expired.  That  this  patient  was  fully  aware  of  his  being  in  daily — 
yes,  hourly — danger  of  death  was  shown  by  the  fact  that  he  had 
given  explicit  directions  to  his  clerk  what  to  do  in  the  event  of 
such  a  fatality.  Reflecting  upon  this  case,  one  cannot  help  won- 
dering by  what  knowledge  this  patient  recognised  the  significance 
of  his  final  attack,  and  refused  to  have  a  medical  man  summoned, 
when  in  previous  attacks  he  had  always  sought  the  services  of  the 
most  accessible  physician. 

The  following  case  is  appended  because  it  emphasizes  in  an 
imjDressive  way  several  points  with  respect  to  aortic  regurgitation. 
In  the  first  place  it  illustrates  the  important  part  played  by  heart- 
strain;  in  the  second,  how  hopeless  is  the  prognosis  in  these  cases; 
thirdly,  the  futility  of  treatment;  and,  lastly,  the  manner  of  death 
in  a  considerable  proportion  of  them. 

I  recently  witnessed  the  death  of  a  gentleman  of  forty-two 
who  had  sought  medical  advice  three  months  before  on  the  sup- 
position that  his  distress  was  due  to  some  form  of  stomach  trouble. 
Excepting  scarlatina  at  the  age  of  six,  he  had  never  known  a  day's 
illness,  and  his  habits  had  been  exemplary  with  the  one  exception 
that  he  had  been  accustomed  to  take  about  two  drinks  a  day  of 
whisky  before  meals.  He  had  always  been  devoted  to  hunting  and 
£shing,  and  had  spent  much  time  each  year  in  the  woods,  at  which 
times  he  had  always  shouldered  his  pack  and  tramped  along  with 
his  guides,  having  many  a  time,  as  he  said,  "  Done  them  up  and 
come  in  at  night  fresh  as  a  daisy,  while  they  were  beat  out."  He 
had  thought  nothing  of  carrying  60  pounds  on  his  back  all  day 
through  the  woods,  and  had  paddled  and  portaged  with  the  best 
of  them.  When  not  out  hunting  or  fishing  he  had  been  untiring 
in  his  devotion  to  business,  and  for  the  previous  seven  years  had 
worked  with  colossal  energy  in  building  up  vast  interests  in  the 
North.  In  addition  to  tireless  work  with  his  brain  in  his  office, 
he  had  endured  and  indeed  revelled  in  efforts  connected  with  his 
business  schemes,  requiring  and  displaying  extraordinary  physical 
endurance,  so  that  he  was  the  marvel  of  his  friends.  On  one  occa- 
sion, in  December,  1900,  this  robust  man  of  medium  stature  and 
weight,  without  an  ounce  of  superfluous  fat,  all  muscle  and  sinew, 
started  with  a  crew  of  men  up  his  railroad  to  inspect  some  work, 
and,  as  the  engine  was  forced  to  "  buck  snowdrifts  "  and  make  a 


310  DISEASES   OF   THE   HEART 

way  for  itself,  the  engineer  suddenly  discovered  that,  having 
neglected  to  fill  his  tank  afresh,  it  was  out  of  water.  The  weather 
was  intensely  cold,  and  this  meant  that  the  fire  would  have  to  be 
dumped  and  the  locomotive  be  allowed  to  freeze  up,  or  that  in 
some  way  a  supply  of  water  must  be  obtained.  They  were  near 
a  river,  and  this  indomitable  man  of  whom  I  write  started  on  a 
dead  run  through  the  deep  snow  for  a  camp  of  his  men  a  mile  and 
a  half  distant,  where  he  knew  he  could  obtain  some  pails.  He 
went  himself  because  he  knew  he  could  get  there  in  quicker  time 
than  any  of  his  men,  and,  too,  would  have  the  authority  to  take  the 
buckets.  Arriving  there,  he  shouldered  a  package  of  half  a  dozen 
iron  buckets  and  started  back,  running  all  the  way  through  the 
snow  with  his  load  of  75  pounds.  He  arrived  in  time  to  save  the 
engine,  but  completely  exhausted.  Xevertheless  he  recovered  in 
the  course  of  the  day,  and  thought  nothing  more  of  it,  going 
about  his  herculean  daily  work  in  and  out  of  the  office  as  before. 
But  outraged  ]S"ature  was  to  have  her  revenge  yet.  In  April  fol- 
lowing his  almost  superhuman  effort,  this  man  of  affairs  took  a 
hard,  fast  horseback  ride  of  ten  miles  over  a  very  rough  road,  and 
before  he  reached  his  destination  he  became  seized  with  a  severe 
pain  in  the  epigastrium,  which,  however,  ceased  to  trouble  him 
greatly  after  he  had  dismounted.  From  that  time  on  until  I  saw 
him  the  next  October,  he  had  grown  steadily  less  and  less  able  to 
endure  exertion  without  this  epigastric  distress,  to  which  dyspnoea 
finally  became  added.  In  June  following  his  ride,  he  had  climbed 
down  and  up  a  ladder  into  and  out  of  a  mine  several  hundred  feet 
in  depth,  and  on  reaching  the  surface  again  had  noticed  that  he 
was  very  much  winded,  and  from  this  time  forward  he  was  obliged 
to  walk  slowly  if  he  did  not  wish  to  suffer  from  his  pain  and  short- 
ness of  breath.  The  night  previous  to  his  arrival  in  Chicago,  and 
on  several  other  occasions,  he  had  been  awakened  in  the  small 
hours  by  a  feeling  of  oppression  which  compelled  him  to  sit  up 
on  the  edge  of  his  bed  and  breathe  hard.  On  this  particular  occa- 
sion he  had  attributed  his  attack  to  the  closeness  of  the  sleeping- 
car,  had  taken  a  drink  of  whisky,  experienced  speedy  relief,  and, 
lying  down,  had  gone  to  sleep.  Such  in  l)riof  was  his  history,  as 
full  of  interest  as  a  romance. 

From  his  recital  I  expected  to  find  a  case  of  simple  cardiac  dila- 
tation from  overstrain,  such  a  case  as  I  had  shortly  before  finished 


AORTIC   REGURGITATION 


511 


treating.  Imagine  my  surprise,  therefore,  when  I  discovered  a 
collapsing  but  not  large  pulse  of  about  .110,  a  diffused,  rather 
indefinite  apex-beat  way  below  and  outside  the  left  nipple,  percus- 
sion evidence  of  a  greatly  hypertrophied  and  dilated  left  ven- 
tricle (Fig.  60),  feeble  heart-sounds,  and  everywhere  a  loud  dou- 
ble murmur  plainly  aortic  in  origin.  Duroziez's  sign  and  capillary 
pulse  were  present,  and  the  liver  was  palpable  and  tender  a 
couple  of  inches  below  the  inferior  costal  margin.  The  left  lobe 
was  specially  swollen  and  sensitive  to  pressure.  The  urine  was 
and  always  remained  negative. 

Here,  then,  was  an  aortic  regurgitation,  but  what  was  its  eti- 
ology ?  Was  it  possible  that  there  had  been  a  valvulitis  years  before 
and  that  the  compensation 
had  been  broken  down  by  his 
prodigious  exertions,  or  had 
the  heart  -  muscle  been  not 
quite  healthy  and  had  that 
run  started  a  stretching  of 
the  aortic  ring  which  had  been 
increased  by  succeeding  ef- 
forts, or  had  the  strain  led 
to  an  aortitis  or  aneurysm, 
and  this  to  insufficiency  of  the 
valves  ?  Rupture  of  a  cusp 
was  out  of  the  question,  be- 
cause of  the  absence  of  serious 
symptoms  in  the  weeks  imme- 
diately succeeding  his  run.  A 
previous  valvulitis  was  not 
impossible,  for  it  is  well 
known  that  the  enormous  secondary  hypertrophy  of  the  left  ven- 
tricle sometimes  developed  in  cases  of  rheumatic  incompetence  of 
the  aortic  valves,  is  capable  of  enduring  an  extraordinary  degree 
of  strain  for  years,  as  witness  some  of  the  cases  treated  by  the 
great  Stokes.  In  this  instance  there  was  no  history  of  anything  to 
lead  to  endocarditis  except  the  scarlatina,  and  that  occurred  thirty- 
six  years  before,  and  if  that  had  led  to  valvular  insufficiency  its 
presence  had  never  been  suspected  or  betrayed  by  a  symptom. 
Moreover,  thirty-six  years  is  a  very  long  time  for  an  aortic  regur- 


FiG.  60. — Relative  Dulness  ix  Case  of 

Aortic  Eeguegitation  (p.  309). 

First  examination. 


312 


DISEASES  OF   THE   HEART 


gitation  to  exist  without  discoverv.  I  therefore  considered  this 
explanation  as  less  likely  than  one  of  the  others.  Regarding  aneu- 
rysm as  cause  of  aortic  ineonn)etenee,  I  had  already  observed  a 
case  in  which  such  was  the  condition,  not  a  very  unusual  one,  but 
for  the  greater  part  of  a  year  there  had  been  no  symptom  to  point 


■■ 

■ 

■ 

^K^B^HBsl^^^^^lwf^ 

^^^^^^^^^^^1 

^^^^H 

^H 

HRRHSn^ 

^^^^1 

^H 

n 

m 

1 

1 

I 
1 

^^^^^^1 

^^^^i^^^^ 

\ 

¥ui.  01. — Skiaouam  ok  (."iiK.-fT  in  Tase  of  Aoijtic  Reourgitation. 

to  aneurysm,  and  it  was  not  discovered  until  three  months  prior  to 
death  from  pressure  on  the  left  lung.  C'onscciuently  I  now  had  a 
Roentgen-ray  ])icture  taken  for  the  <l('tection  of  aneurysm  if  such 
existed.     It  is  sliown  above  (Fig.  til),  aiid  shows  great  breadth 


AORTIC  "REGURGITATION  313 

of  shadow  at  the  base  over  the  j^osition  of  the  large  vessels,  but 
nothing  that  can  be  interpreted  to  indicate  aneurysm.  It  also 
shows  a  very  large  heart,  a  veritable  co?^  hovinum.  The  only  re- 
maining hypothesis  was  that  of  stretching  of  the  aortic  ring  and 
base  of  the  aorta.  The  vessel  could  be  felt  pulsating  at  the  level 
of  the  upper  edge  of  the  sternum,  and  in  the  aortic  area  could 
be  heard  a  faint  distinct  click,  evidently  a  feeble  aortic  second 
tone. 

Another  case  that  has  been  already  narrated  (see  page  158) 
had  taught  me  how  guarded  one  should  be  in  attributing  to  endo- 
•carditis  what  might  turn  out  to  be  attributable  to  myocarditis  and 
stretching  of  the  orifice,  especially  in  the  absence  of  a  definite  his- 
tory of  rheumatism  or  other  sufficient  etiological  factor.  In  the 
present  instance  this  point  was  of  great  importance  in  its  bearing 
on  prognosis.  I  believe  the  subsequent  lack  of  resistance  on  the 
part  of  the  left  ventricle  bore  out  strongly  my  original  view  of 
the  origin  of  the  valvular  incompetence.  The  leak  was  started 
by  the  awful  strain  of  that  insane  run,  and  was  augmented  and 
rendered  hopeless  of  repair  by  his  succeeding  exertions. 

The  man  was  told  how  serious  his  condition  was,  and  that  his 
only  hope  of  reinstating  his  heart-power  lay  in  at  once  giving  him- 
self up  to  entire  and  prolonged  rest  in  bed.  Very  reluctantly  he 
yielded  to  the  inevitable,  and  took  to  his  bed.  He  was  of  a  some- 
what peculiar  nervous  make-up  and  could  not  be  induced  to  remain 
as  inactive  as  I  thought  was  necessary.  He  would,  for  instance, 
get  up  and  go  to  the  toilet  in  the  adjoining  bath-room  instead  of 
using  a  bed-j)an.  He  would  get  up  and  shave  himself,  and  he 
would  sit  up  in  bed  to  eat,  and  on  one  or  two  occasions  arose  to 
receive  a  visitor.  I  now  blame  myself  for  having  permitted  even 
so  much  latitude,  yet  his  annoying  symptoms  disappeared  so 
promptly  on  being  put  to  rest  and  his  left  ventricle  came  down 
so  appreciably  in  size  and  the  apex-beat  returned  in  such  strength, 
that  I  hoped,  against  my  first  judgment,  that  the  heart  was  going 
to  recover  its  hypertrophy  better  than  was  at  first  feared. 

At  the  end  of  a  month  of  this  enforced  inaction  the  patient  be- 
came so  restless  that  permission  was  given  him  to  leave  his  bed 
and,  by  degrees,  begin  to  move  about,  under  the  condition  that  he 
was  to  lie  down  much  of  the  time.     He  was  allowed  also  to  take 

a  daily  drive.     A  course  of  Nauheim  baths  was  also  begun  in  the 

22 


314  DISEASES  OP  THE   HEART 

hope  of  re-enforcing  the  effect  of  the  digitalis,  nitroglycerin,  and 
strychnine  he  was  taking.  For  a  week  he  did  not  seem  to  suffer 
any  ill  consequences,  although  he  ignorantly  overdid  in  various, 
to  him,  seemingly  trivial  ways.  He  would  jDut  on  his  heavy  fur- 
lined  overcoat  unassisted,  and  go  into  a  store  to  make  purchases, 
and  be  on  his  feet  for  an  hour  at  a  time,  not  realizing  that  he 
was  still  far  from  well.  Then  the  saline  baths  did  not  slow  his 
pulse  and  improve  its  quality  as  they  should  have  done,  and 
after  a  bath  he  did  not  react  to  my  satisfaction.  So  after  two 
weeks,  in  which  it  was  clear  that  he  was  losing  ground,  I  again 
ordered  him  to  bed,  this  time  insisting  on  his  having  a  trained 
nurse  who  was  to  lift  him,  and  in  many  w^ays  save  him  from  efforts 
he  had  made  during  the  earlier  weeks.  He  now  remained  fairly 
quiet,  though  it  was  very  difficult  for  him  to  learn  to  keep  still 
and  not  to  assist  his  nurse  whenever  she  lifted  him,  turned  him, 
etc.  He  simply  would  not  use  a  bed-pan,  and  therefore  was  drawn 
in  a  chair  to  the  bath-room,  and  later  on  was  lifted  on  to  a  night- 
stool  alongside  his  bed.  His  treatment  consisted  of  digitalis  and 
other  tonics,  cathartics,  and  resistance  exercises  given  by  a  com- 
petent attendant.  Although  it  was  realized  that  these  last  were 
in  violation  of  the  jirinciple  of  absolute  physical  repose,  still  they 
were  decided  on  because  they  slowed  the  pulse  somewhat,  im- 
proved its  quality,  and  so  quieted  him  that  he  fell  asleep  after  the 
seance  was  over.     Xo  more  Xauheim  baths  were  given. 

As  days  ran  into  weeks,  however,  it  became  plain  to  me  that 
treatment  was  not  going  to  restore  what  he  had  lost  during  the 
two  weeks  he  had  been  up.  Indeed,  he  slowly  but  perceptibly  lost 
ground.  His  liver  swelled  again  somewhat  and  gave  a  very  uncom- 
fortable feeling  of  fulness  below  the  ribs,  which  he  attributed  to 
his  stomach  and  to  indigestion.  The  outline  of  the  left  ventricle 
very  gradually  became  more  rounded,  the  apex  less  pointed,  and 
its  impulse  less  vigorous.  It  was  at  length  clear  that  if  the  mitral 
valve  was  not  already  relatively  incompetent,  a  matter  for  cer- 
tain reasons  difficult  of  positive  determination,  it  would  soon  be- 
come so. 

January  1st  he  was  moved  from  the  hotel  into  a  rented  house, 
and  the  removal  was  effected  as  easily  and  with  as  little  disturbance 
to  him  as  possible.  Nevertheless  when  I  visited  him  a  few  hours 
later  I  saw  at  once  that  the  transfer  had  Imrt  liim.     His  pulse  was 


AORTIC  REGURGITATION  315 

less  strong,  the  heart-dulness  a  little  larger,  and  his  breathing  a 
little  less  easy. 

The  feature  that  especiall}''  increased  my  anxiety,  hoAvever,  was 
the  peculiar  irregularity  of  the  pulse.  At  varying  intervals,  from 
5  to  20  beats,  there  would  come  a  sudden  quick  wave  closely  fol- 
lowing the  one  before,  as  if  the  heart  were  trying  to  catch  up  in  its 
work  by  giving  an  extra  contraction  {pulsus  intercuri'ens).  The 
patient,  moreover,  appeared  totally  unconscious  of  this  peculiar 
action,  which  did  not  disappear  during  the  remaining  two  weeks 
of  life  until  the  dilatation  of  the  left  ventricle  had  grown  so  ex- 
treme as  to  lead  to  relative  incompetence  of  all  the  other  valves. 
One  night,  apparently  in  consequence  of  flatulent  distention  of 
the  bowels,  he  became  extremely  nervous  and  alarmed  over  a  flut- 
tering of  the  heart,  which  persisted  for  several  hours,  and  until 
after  a  dose  of  whisky  administered  by  the  nurse  he  fell  asleep. 

To  add  to  the  damaging  effect  of  all  this  strain,  the  patient 
became  nervous  and  despondent,  and  so  desirous  of  getting  out  of 
doors  that  I  agreed  to  his  going  out  in  his  wheel-chair  provided 
he  was  carried  downstairs  on  a  stretcher,  then  placed  in  his  chair, 
and  on  his  return  brought  up  again  in  the  same  manner.  This 
was  attempted  but  was  bungled  in  some  way  so  that  he  was  ren- 
dered extremely  nervous,  and,  after  all,  was  borne  down  and  up 
in  his  attendant's  arms.  This  in  reality  ought  not  to  have  injured 
him  had  his  heart-muscle  been  less  seriously  damaged.  As  it 
was  I  recognised,  so  soon  as  I  examined  him  a  short  time  after- 
ward, that  the  walls  of  the  cardiac  cavities  were  still  more 
stretched  and  the  liver  still  more  engorged. 

He  now  lost  his  appetite  entirely,  passed  rather  poor  nights, 
and  showed  a  slight  pufliness  of  the  insteps.  One  week  later  he 
began  to  have  very  slight  nausea,  and  on  Sunday  forenoon  was 
seized  with  a  sudden  attack  of  vomiting.  He  rose  up  in  bed  and 
strained  violently  in  the  act  in  a  way  to  make  me  most  uneasy.  I 
happened  to  be  sitting  by  his  bedside  at  the  time  and  took  occasion 
to  observe  the  pulse.  This  did  not  become  specially  accelerated 
but  rather  thready,  and  its  irregularity  somewhat  more  pro- 
nounced. Examination  of  the  heart  did  not,  however,  reveal  any 
marked  ill  effect.  He  was  now  put  on  kumyss,  and  all  internal 
medication  was  stopped  lest  the  stomach  might  be  again  disturbed. 
He  passed  a  poor  night  and  the  next  day  complained  of  rather 


316 


DISEASES   OF   THE   HEART 


more  fulness  in  the  epigastrium.  About  noon  this  feeling  of  dis- 
tress increased,  a  "  hard  lump  "  appeared  above  the  umbilicus,  and 
about  4  p.  ii.  he  had  a  prolonged  nervous  chill.  They  succeeded 
in  reaching  me  by  telephone  at  this  time,  and  I  ordered  an  injec- 
tion of  morphine  -^  with  jjo  *^*^  atropine,  thhiking,  as  considered 

by  the  nurse,  that  the  pain 
and  "  knotting  "  might  be  an 
accumulation  of  flatus  in  the 
colon.  Upon  arriving  an  hour 
later  and  examining  the  abdo- 
men, I  at  once  discovered  that 
the  left  lobe,  of  the  liver  was 
greatly  swollen,  tender  to 
pressure,  and  was  throbbing 
from  the  propagated  pulsa- 
tion of  the  aorta  beneath.  It 
required  only  a  brief  exami- 
nation of  the  heart  to  perceive 
that  the  strain  of  vomiting  the 
day  before  had  done  its  evil 
work  by  setting  up  a  marked 
increase  of  back-pressure  (Fig. 
62).  The  external  jugulars 
were  swollen,  the  right  heart  more  dilated,  and  the  pulmonic  sec- 
ond tone  very  muffled.  A  cathartic  was  ordered  and  he  was  at 
once  put  on  a  hypodermic  of  nitroglycerin  j^  with  -^\  of  strych- 
nine sulphate  every  four  hours.  Half  a  dozen  watery  stools  the 
next  morning  made  him  feel  comfortable,  but  it  was  clear  that 
back-pressure  was  on  the  increase.  By  noon  he  was  quite  cyanosed, 
and  the  pulse  was  small  and  weak.  He  was  then  put  on  15  drops 
of  fat-free  tincture  of  digitalis  every  two  hours,  the  glonoin, 
strychnine,  and  cathartics  being  continued. 

Wednesday  morning,  in  s})ite  of  free  hydragogne  catharsis, 
his  condition  was  still  worse.  The  pulmonic  second  tone  was  re- 
placed by  a  soft  diastolic  murmur,  and  he  was  cyanosed.  Even 
turning  him  in  bed  produced  profound  cyanosis,  feebleness  of  the 
pulse,  and  difficulty  of  breathing.  The  morphine  was  continued 
hypodermically  in  doses  of  ^  once  or  twice  in  twenty-four  hours  to 
prevent  restlessness  and  unnecessary  suffering,  while  the  interval 


Fiu.  62. — Relative  Dvlness  and  Lowek 
Border  of  Liver  shortly  before 
Death.    Same  case  as  Figs.  60  and  61. 


AORTIC*  REGURGITATION  317 

between  the  injections  of  nitroglycerin  and  strychnine  was  short- 
ened to  two  instead  of  four  hours.  He  then  rallied  for  a  few 
hours  and  the  cyanosis  almost  disappeared,  but  the  heart-findings 
remained  about  as  before.  Morphine  gave  him  a  fairly  comfort- 
able night  and  Thursday  came.  The  pulmonic  second  sound  was 
now  audible  again,  but  the  pulmonic  diastolic  murmur  persisted 
and  the  external  jugulars  and  liver  pulsated  unmistakably,  while 
a  soft  systolic  bruit,  evidently  tricuspid,  could  be  heard  at  right 
of  the  sternum  near  its  extremity. 

The  pulse  now  began  to  slow  down,  from  96  to  90,  then  to  88, 
and  by  noon  to  80,  yet  did  not  grow  stronger.  On  the  contrary, 
it  seemed  to  grow  smaller  and  weaker,  while  the  jugular  pulsation 
increased,  and  distention  of  the  right  auricle  caused  absolute  dul- 
ness  to  reach  across  the  sternum  and  beyond.  He  had  now  re- 
ceived 24  doses  of  digitalis,  and  believing  that  it  would  only  do 
still  greater  harm,  I  ordered  it  stopped  and  provided  elixir  of 
valerianate  of  ammonia  and  a  10-per-cent  solution  of  camphor  in 
sterilized  olive  oil  against  possible  further  sinking  of  the  j)ulse. 
The  oil  was  to  be  injected  under  the  skin  in  case  of  need. 

The  feet  and  ankles  were  now  quite  oedematous,  urine  was  very 
scant,  the  patient  persj)ired  profusely,  slept  much  of  the  time,  and 
was  profoundly  cyanosed  with  marked  pufSness  of  the  neck  and 
lower  part  of  the  face.  More  bowel  movements  of  a  watery  charac- 
ter were  secured  without  any  impression  on  the  stasis.  The  pulse 
stayed  at  80,  very  weak,  and  whenever  to  rest  him  he  was  turned 
on  to  his  back  or  left  side,  became  distinctly  worse.  His  greatest 
comfort  was  when  he  lay  in  the  right  lateral  decubitus.  His 
respirations  were  28,  and  his  breathing  was  laboured  at  'times. 
Rales  of  hypostatic  congestion  were  audible  at  the  right  base 
behind. 

In  this  condition  things  remained  until  10.30  p.  m.,  when  sud- 
denly he  complained  of  inability  to  breathe,  turned  purple  in  the 
face,  grew  rigid  and  pulseless.  The  nurse  hastily  injected  the 
camphorated  oil  as  I  entered  the  room  and  hurried  to  the  bedside. 
I  listened  for  the  heart-sounds,  but  all  was  still;  life  was  extinct, 
his  mwscles  relaxed  and  his  sufferings  were  at  an  end. 

This  case  has  been  detailed  at  this  length  in  the  belief  that  it 
might  prove  highly  instructive  on  many  of  the  points  that  have 
been  already  dwelt  upon  in  regard  to  aortic  regurgitation,  and 


318  DISEASES  OF   THE   HEART 

will  be  dwelt  on  in  considering  the  prognosis  and  treatment  of 
valvular  disease  in  general. 

It  brings  out  only  too  clearly  the  utter  hopelessness  of  the  prog- 
nosis in  aortic  insufficiency  in  men  of  middle  age  when  compensa- 
tion once  gives  way,  no  matter  what  the  cause  of  the  valvular  de- 
fect. The  heart-walls  are  too  degenerated  to  retain  any  temporary 
improvement  that  may  follow  appropriate  treatment. 

In  the  matter  of  management  nothing  is  so  important  as  rest, 
and  this  should  be  as  absolute  as  possible.  One  cannot  refrain  from 
looking  over  his  management  of  a  case  and  being  inclined  some- 
times to  upbraid  himself  for  not  having  done  this  or  that.  In  this 
case  I  now  think  I  should  perhaps  have  been  rather  more  energetic 
with  digitalis  from  the  very  start  than  I  -was,  and  yet  at  the  time  I 
feared  its  effects  on  the  vascular  system  might  offset  that  on  the 
heart.  In  another  case  I  believe  I  will  try  pushing  the  drug  to  the 
limit  of  its  usefulness.  Then  as  to  the  degree  of  rest  which  was 
secured.  I  might  have  been  less  lenient,  and  yet  this  gentleman 
had  been  so  active  a  man  that  rest  in  bed  chafed  him.  It  was  a 
nice  question  to  decide  whether,  as  a  matter  of  fact,  strictness  in 
regard  to  complete  physical  inaction  would  not  have  made  him  so 
impatient  and  restless  in  spirit  as  to  have  entirely  counteracted  the 
benefit  to  be  had  from  rest  of  body,  or  as  to  have  done  him  greater 
harm  than  did  the  little  exercise  he  took  during  the  first  month 
of  treatment.  At  all  events  this  was  how^  I  looked  at  it  then,  and 
I  am  not  sure  but  I  w^as  right.  As  a  matter  of  fact  the  result  was 
inevitable,  and  no  treatment  could  do  more  than  retard  the  fatal 
issue. 


CHAPTER    IX 
AORTIC    STENOSIS 

This  is  a  comparatively  rare  affection  when  existing  alone, 
and,  as  its  name  signifies,  consists  of  a  narrowing  of  the  aortic 
ostium.  It  is  aways  a  structural  defect  and  owes  its  origin  chiefly 
to  inflammatory  changes. 

Morbid  Anatomy. — There  are  two  types  of  structural 
change  that  may  lead  to  narrowing  of  the  aortic  orifice:  (1)  The 
cusps  of  the  valve  may  become  adherent  and  stiffened;  (2)  growth 
and  organization  or  calcification  of  vegetations  may  take  place  in 
such  a  way  as  to  interfere  with  the  passage  of  the  blood-stream. 
The  former  defect  may  be  due  to  a  developmental  error,  and  oc- 
curs in  congenital  narrowing.  It  inay  also,  however,  follow  acute 
endocarditis.  The  cusps  may  become  so  completely  adherent  that 
only  a  small  opening,  scarcely  large  enough  to  admit  the  point  of 
a  lead-pencil,  is  left.  Fig.  63  shows  such  a  heart,  and  also  illus- 
trates the  proneness  of  acute  endocarditis  to  attack  a  valve  already 
the  subject  of  chronic  disease.  Here  a  tiny  row  of  vegetations  is 
seen  along  the  line  of  maximum  contact  during  the  closure  of  the 
valves.  In  those  cases  of  stenosis  of  sclerotic  origin  in  which  the 
cusps  are  not  adherent  but  interfere  with  the  blood-flow  on  ac- 
count of  stiffness  which  prevents  their  swinging  back  in  the  normal 
way,  regurgitation  is  usually  so  freely  permitted  that  the  case  is 
classed  as  one  of  insufficiency. 

In  the  second  class,  vegetations  on  the  aortic  valve  may  assume 
such  proportions  as  to  induce  narrowing  of  the  orifice.  These  oc- 
cur most  usually  on  the  ventricular  surface  of  the  valve  segments, 
and  in  that  situation  of  course  interfere  also  with  the  closure  of 
the  valve,  producing  leakage.  The  narrowing  is  usually  the  pre- 
dominant effect,  however,  of  a  large  vegetation  in  this  situation. 
An  interesting  type  of  stenosis,  shown  well  in  Fig.  64,  is  that  in 
which  vegetations  develop  in  one  or  more  of  the  sinuses  of  Yal- 

319 


320 


DISEASES   OF   THE   HEART 


sah'a.  Calcified  thrombi  in  this  location  almost  completely  pre- 
vent the  opening  of  the  valve,  and  may  produce  an  extreme  grade 
of  stenosis. 


Fig.  63. — Heart  of  Aortic  Stenosis,  with  Auheisent  Aortic  Cusps,  ank  also 
Acute  Endocarditis. 


Aortic  stenosis  is  not  always  located  in  the  valve,  however,  for 
the  aortic  ring,  and  sometimes  the  wh(jle  trunk  of  the  vessel,  may 
he  narrowed.  This  is  prohaldy  most  often  a  congenital  defect. 
Stenosis  of  the  licart,  or  iiioro  ])i'o])erly  of  the  conns  arteriosus  of 
the  left  ventricle,  may  also  jjrodncc  the  sccondiiry  effects  of  ste- 
nosis of  the  orifice. 

It  goes  without  saying  that  a()rti(;  stenosis,  accoi'ding  to  its  de- 
gree, presents  more  (»r  Ic^-  resistance  lo  the  dutllow  of  Mood  from 


AORtiC  STENOSIS 


}21 


the  ventricle.  In  order,  therefore,  to  discharge  a  normal  volume 
of  blood  through  the  diminished  opening,  the  ventricle  is  obliged  to 
contract  more  powerfully  and  more  slowly.  This  increased  work 
results  in  the  development  of  hypertrophy. 

Fraentzel  is  of  the  opinion  that  dilatation  of  the  ventricular 
cavity  precedes  the  hypertrophy,  because  the  wall  cannot  accom- 
modate itself  to  its  increased  task.  This  would  be  the  case,  doubt- 
less, were  the  stenosis  suddenly  developed,  but  inasmuch  as  the 
changes  in  the  valves  leading  to  stenosis  are  brought  about  slowly, 
the  wall  of  the  left  ventricle  is  able,  pari  passu,  to  meet  the  grow- 


*^  '^jjSt 


Fig.  64. — Heart  of  Aortic  Stenosis,  showing  Calcified  Vegetations  in  Sinuses 

OF  Valsalva. 


ing  resistance.    It  seems  clear,  therefore,  that  hypertrophy  of  the 
left  ventricle  is  the  first  result :  and  that  when  dilatation  of  its 


322  DISEASES  OF  THE   HEART 

cavitj  is  also  present,  it  is  either  the  effect  of  associated  regurgita- 
tion or  comes  on  gradually  with  failing  compensation. 

Until  compensation  does  fail  the  secondary  effects  are  limited 
to  the  left  ventricle.  When,  however,  the  ventricle  becomes  un- 
able to  fully  empty  itself  at  each  systole,  the  residual  blood  forms 
an  obstruction  to  the  complete  emptying  of  the  auricle.  The  stasis 
thus  produced  creeps  back  in  the  manner  already  described  in  pre- 
ceding chapters,  with  the  result  of  general  cardiac  enlargement, 
and  the  manifestations  of  passive  congestion  in  the  various  organs 
of  the  body. 

In  extreme  grades  of  stenosis  the  supply  of  blood  to  the  coro- 
nary arteries  may  be  so  reduced  as  to  cause  degeneration  of  the 
myocardium.  In  this  manner  the  constriction  tends  ultimately 
to  the  destruction  of  that  compensatory  hypertrophy  by  which 
alone  the  effects  of  the  stenosis  can  be  offset.  It  will  be  readily 
seen  that  in  such  a  heart  as  that  of  Fig.  64,  this  factor  would  be 
of  great  importance. 

Etiology. — Stenosis  of  the  aortic  orifice  is  in  nearly  all  in- 
stances acquired  after  birth  and  is  then  due  either  to  endocarditis 
or  sclerosis.  The  disease  occurs  more  often  in  the  male  than  the 
female  sex,  the  same  as  aortic  regurgitation,  and,  in  my  experience, 
more  frequently  in  the  young.  It  is,  however,  so  rarely  observed 
independently  of  incompetence  that  of  several  hundred  cases  of 
valvular  disease  of  which  I  have  records,  there  are  only  half  a 
dozen  instances  of  pure  and  uncomplicated  stenosis  of  the  kind 
under  consideration.  This  is  readily  understood  when  one  reflects 
for  a  moment  upon  the  conditions  which  are  responsible  for  the 
stenosis. 

In  those  cases  in  which  the  valve-segments  are  agglutinated 
and  rigid,  projecting  like  a  cone  into  the  lumen  of  the  artery,  there 
is  left  a  small  opening  at  the  extremity  of  the  cone  through  which 
a  certain  amount  of  reflux  is  possible.  In  other  cases  in  which  vege- 
tations cause  obstruction  there  is  usually  such  a  condition  of  the 
thrombi  or  of  the  valve-flaps  as  prevents  their  perfect  coapta- 
tion, and  hence  regurgitation  takes  place. 

When  in  any  given  case  regurgitation  is  not  also  recognised 
clinically,  the  conclusion  is  reasonal)lo  that  either  tlie  valve  is  not 
too  rigid  to  close  the  ostium,  or  that  the  seat  of  obstruction  is  in 
the  ring  or  conus. 


AORTIC  STENOSIS  323 

The  etiological  factors  responsible  for  the  endocarditis  or  the 
degenerative  changes  underlying  the  stenosis  have  already  been 
so  fully  considered  in  the  causation  of  the  foregoing  valvular  de- 
fects that  it  would  be  a  needless  repetition  to  discuss  them  here. 

Symptoms. — Stenosis  of  an  orifice  is  justly  regarded  as  a 
serious  affection ;  yet  in  this  particular  lesion  subjective  symptoms 
are  sometimes  entirely  wanting.  Consequently  the  clinical  fea- 
tures of  each  case,  as  well  as  their  severity,  depend  upon  the  de- 
gree of  narrowing.  If  this  is  extreme,  it  is  impossible  for  the 
disease  to  remain  latent,  and  the  patient  suffers  either  from  a  too 
inadequate  supply  of  arterial  blood  to  maintain  nutrition  and  nor- 
mal visceral  function,  or  from  the  effects  of  stasis  behind  the  seat 
of  constriction. 

In  the  slighter  degrees  of  aortic  stenosis  patients  are  usually 
capable  of  ordinary  physical  and  mental  activity  the  same  as  their 
companions.  I  recall  a  lad  of  fifteen  who  presented  himself  at  my 
clinic  in  the  Post-Graduate  Medical  School,  because  of  some  trivial 
digestive  disorder,  and  in  whom  were  discovered  all  the  signs  of 
uncomplicated  aortic  stenosis.  Judged  by  the  secondary  physical 
signs  it  was  not  very  pronounced,  and  the  boy  stated  that  he  was 
a  newsboy  selling  papers  on  the  suburban  trains,  in  the  habit  of 
carrying  heavy  bundles  of  papers,  and  of  jumping  on  and  off  mov- 
ing trains  without  any  shortness  of  breath  or  consciousness  of  his 
heart's  action. 

It  is  in  such  cases  as  this  that  individuals  go  for  years  without 
knowing  there  is  anything  wrong  with  them,  and  at  length  learn 
of  their  defect  through  its  accidental  discovery  by  some  medical 
examiner.  Indeed,  persons  with  thoroughly  compensated  aortic 
obstruction  may  pass  through  their  entire  lives  to  old  age  without 
having  ever  learned  of  their  disease.  The  pulse  of  such  an  indi- 
vidual is  slower  and  smaller  than  normal,  and  the  cardiac  impulse 
denotes  hypertrophy,  but  having  grown  up,  so  to  speak,  with  these 
deviations  from  the  general  rule,  he  pays  them  no  attention. 

If  any  circulatory  disturbances  result  from  the  aortic  constric- 
tion when  single  and  of  minor  degree,  they  are  such  as  indicate 
deficient  supply  of  arterial  blood  to  the  various  organs  and  parts 
of  the  body.  Even  these  effects  may  be  too  slight  to  attract  special 
attention.  At  the  most,  the  circulation  is  not  very  active,  and  the 
boy  may  not  be  quite  as  vigorous  as  his  healthy  play-fellows. 


324  DISEASES  OF   THE   HEART 

It  is  stated  by  some  authors  that  aortic  narrowing  of  consider- 
able degree  may  occasionally  give  rise  to  distinct  symptoms  of  cere- 
bral anaemia — i.  e.,  syncopal  attacks  and  epileptiform  seizures. 
Such  serious  effects  must  indicate  either  an  extreme  grade  of  ob- 
struction or  periods  of  cardiac  weakness  when  the  left  ventricle 
expels  very  small  amounts  of  blood,  or  perhaps  none  at  all,  for  a 
few  seconds,  in  consequence  of  intermittence.  A  far  more  common 
symptom  is  vertigo ;  and  yet  even  in  this  there  is  nothing  peculiar 
to  aortic  stenosis,  since,  as  well  known,  dizziness  may  be  experi- 
enced in  any  form  of  valve-lesion.  In  one  instance  coming  under 
my  observation  attacks  of  vertigo  proved  a  most  distressing  fea- 
ture, and  yet  in  this  case  they  depended  not  so  much  upon  the 
cardiac  defect  per  se  as  upon  disordered  action  of  the  muscle  fibres 
— i.  e.,  interference  with  its  capacity  for  conducting  motor  im- 
pulses. The  case  presents  features  that  bring  it  into  the  category 
of  Stokes-Adams  disease,  and  will  be  referred  to  again  in  con- 
sidering that  interesting  symptom-coni])l('x. 

In  the  fall  of  1899  an  officer  of  the  United  States  Army  de- 
sired my  opinion  concerning  the  condition  of  his  heart,  which  he 
stated  was  very  unusual.  He  was  highly  intelligent,  and  had  made 
his  heart  an  object  of  much  study.  From  his  detailed  report  of 
his  history  the  following  summary  is  given:  He  was  born  in  1873, 
and  with  exception  of  measles  had  no  illness  until  his  eighth  year, 
at  which  time  he  had  a  protracted  and  nearly  fatal  illness 
thought  to  be  acute  gastritis.  For  a  number  of  years  thereafter 
his  digestion  was  weak,  but  he  was  able  to  participate  in  the 
games  and  sports  of  his  playmates  without  being  conscious  of  ill 
effects. 

At  the  age  of  fourteen  or  fifteen  he  accidentally  discovered 
that  his  pulse-rate  was  between  40  and  45,  but  at  the  age  of  eight- 
een he  was  passed  for  life  insurance,  the  examiner  finding  his 
pulse  of  normal  frequency,  and  not  detecting  any  cardiac  murmur. 
Nevertheless,  when  a  year  later  he  applied  for  admission  to  the 
West  Point  Military  Academy  he  was  told  that  he  gave  signs  of 
slight  aortic  stenosis.  •Thereu])on  he  consulted  many  physicians 
in  his  native  town  and  elsewhere,  receiving  a  variety  of  opinions. 
Some  declared  he  had  valvular  disease,  and  others  as  positively 
asserted  the  contrary. 

On  one  occasion,  after  having  hopped  up  and  down  the  exam- 


AORTIC  STENOSIS  325 

iniiig  surgeon's  office,  he  was  told  that  his  pulse  was  beating  140 
per  minute.  To  make  a  long  story  short,  it  suffices  to  say  he  was  at 
length  admitted  to  the  Academy  at  the  age  of  twenty,  notwith- 
standing the  discovery  of  his  aortic  stenosis,  the  lesion  being  con- 
sidered trifling  and  compensation  good.  During  his  cadetship  he 
was  able  to  endure  the  arduous  drills  with  apparently  no  more  dis- 
tress than  did  his  comrades,  although  he  noticed  upon  a  few  occa- 
sions that  the  veins  on  his  forehead  stood  out  prominently. 

In  his  senior  year  he,  like  many  others  of  his  class,  had  to  go  to 
the  hospital  with  chills  and  fever  that  were  considered  malarial, 
and  which  have  not  recurred  since  his  leaving  the  Academy.  From 
September,  1897,  until  the  spring  of  1899,  he  was  stationed  in 
San  Francisco,  and  while  there  had  a  pulse-rate  of  38,  but  with  the 
exception  of  slight  blurring  of  vision  and  headache,  that  was  al- 
ways relieved  by  calomel,  he  had  no  illness  or  symptoms  referable 
to  his  heart.  In  the  fall  of  1898,  upon  being  examined  for  promo- 
tion, he  was  told  he  had  aortic  stenosis  and  mitral  regurgitation, 
and  was  rejected  in  consequence.  ISTevertheless,  upon  his  record 
he  at  length  obtained  his  promotion,  and  was  transferred  to  a  post 
in  the  East. 

In  May,  1899,  he  participated  in  a  bicycle  ride,  being  unac- 
customed to  that  particular  form  of  exercise,  although  he  engaged 
in  every  other  kind  of  sport  and  game  with  his  fellows.  During 
this  ride  he  made  a  spurt,  and  then  got  out  of  breath,  but  other- 
wise appeared  to  suffer  no  inconvenience.  Two  hours  subsequent 
to  his  return  to  his  quarters,  and  while  standing  by  a  table  waiting 
for  dinner,  he  suddenly  became  dizzy  and  was  assisted  to  a  couch. 
The  junior  surgeon  was  summoned,  and  finding  his  pulse  30,  ad- 
ministered whisky,  which  somewhat  relieved  him  and  brought  his 
pulse  up  to  50.  From  that  time  on  he  was  daily  distressed  by  spells 
of  vertigo  for  some  weeks,  and  he  noted  that  the  regular  slow  ac- 
tion of  the  heart  was  every  now  and  then  exchanged  for  a  more 
rapid  irregular  one,  with  an  occasional  violent  thump  against  the 
chest-wall.  At  this  time  his  dizziness  was  usually  relieved  by 
assuming  the  recumbent  posture. 

He  received  some  medicinal  treatment,  nature  unknown,  and 
then  for  a  month  was  free  from  his  distressing  symptom.  It  re- 
turned again,  however,  more  violently  and  still  annoyed  him  in 
November,  1899,  the  date  of  my  first  examination.     During  the 


326  DISEASES  OF  THE  HEART 

summer  previous  lie  was  given  digitalis  for  a  short  period,  and 
twice  after  having  taken  the  remedy  his  pulse  suddenly  became 
accelerated  to  60,  and  was  regular.  During  these  months  he  was 
in  the  habit  of  striving  to  either  work  off  or  forget  his  dizziness  by 
playing  golf,  and  it  is  worthy  of  note  that  such  exercise  did  not 
aggravate  the  symptom. 

In  September,  1899,  he  suddenly,  while  studying  the  action 
of  his  heart,  made  the  discovery  that  during  his  spells  of  vertigo, 
and  while  his  radial  pulse  was  but  26  to  30,  he  could  perceive  by 
placing  his  finger  above  the  clavicle  a  series  of  "  small  pulsations 
which  corresponded  Vv'ith  feeble  heart  contractions."  These  were 
of  variable  number,  and  were  interposed  between  two  energetic 
cardiac  contractions  which  were  declared  by  a  forcible  apex-impulse 
and  by  the  radial  pulse.  He  furthermore  noted  that  no  matter 
how  slow  his  radial  pulse  was,  even  as  infrequent  as  19  in  the  min- 
ute, he  was  not  dizzy  provided  it  was  regular  and  the  number  of 
small  pulsations  in  the  neck  was  uniform.  I  shall  recur  to  this 
striking  and  peculiar  feature  again.  During  that  same  fall  he 
was  treated  for  a  few  weeks  in  the  Battlecreek  Sanitarium,  and 
while  there  requested  on  one  occasion  that  an  "  ice  compress  "  be 
placed  upon  his  heart.  This  was  done,  and  upon  its  removal  ten 
or  fifteen  minutes  later  his  heart  grew  regular  and  the  pulse  at 
the  wrist  registered  56.  He  then  fell  asleep,  only  to  find  next 
morning  that  its  rate  was  again  26  to  30. 

The  night  before  consulting  me  had  been  an  unusually  bad  one, 
and  when  I  saw  him  the  pulse  was  36  and  irregular.  He  admitted 
no  shortness  of  breath  on  exertion,  but  suffered  from  constipation. 
He  thought  that  on  a  few  occasions  he  had  lost  consciousness.  Not 
to  make  this  narrative  tedious,  I  will  say  my  examination  revealed 
hypertrophy  of  the  left  ventricle,  the  apex-beat  when  felt  being 
broad  and  strongly  thrusting  in  the  sixth  left  interspace,  11.5  cen- 
timetres to  the  left  of  the  median  line  and  1  centimetre  outside  of 
nipjde.  Increase  of  both  superficial  and  deep-seated  dulness  to  the 
right  showed  enlargement  of  the  right  heart.  There  was  a  loud, 
rough  systolic  murmur  over  the  entire  pra?cordia  whenever  the 
heart  made  an  energetic  contraction,  and  this  murmur  was  suc- 
ceeded by  a  distinct  second  sound  even  in  the  aortic  area.  Upon  in- 
vestigating this  In-uit  minutely  it  was  found  to  have  two  areas  of 
maximum  intensity,  one  in  the  aortic  and  the  other  in  the  mitral 


AORTIC  STENOSIS  327 

area,  although  I  could  not  detect  that  the  quality  in  the  two  re- 
gions was  diiferent.  I  found  subsequently,  however,  that  at  the 
apex  the  murmur  was  softer  and  more  blowing. 

The  murmur  at  the  base  was  transmitted  upward  into  the  neck 
as  well  as  on  to  the  body  of  the  heart,  while  that  at  the  apex  was 
propagated  outward  into  the  axilla  and  feebly  to  the  back.  At 
first  I  did  not  observe  the  small  pulsations  in  the  neck,  but  when 
my  attention  was  directed  to  them  I  perceived  them  distinctly 
enough,  and  I  also  noted  that  synchronous  with  these  were  feebly 
audible  cardiac  tones,  while  at  a  much  later  date  these  feeble 
heart-sounds  were  accompanied  by  a  faint  murmur  and  an  indis- 
tinct apex-beat.  These  small  pulsations,  for  lack  of  a  better  term, 
were  of  irregular  number,  being  ordinarily  two,  but  sometimes 
as  many  as  seven,  and  according  to  the  officer  even  more,  before 
there  would  come  a  normal  pulse-wave.  It  was  suggested  by  the 
patient  that  these  were  auricular  in  origin,  but  I  decided  that  they 
were  due  to  feeble  ventricular  contractions,  and  subsequent  car- 
diograms taken  by  Dr.  Janeway  in  New  York  established  the  cor- 
rectness of  my  opinion. 

The  very  interesting  feature  pertaining  to  these  incomplete 
systoles  was,  that  so  long  as  they  were  regular  and  in  groups  of 
two,  vertigo  did  not  ensue.  When,  on  the  contrary,  they  ran  up 
to  half  a  dozen  or  more  the  patient  felt  dizzy  or  even  fainted. 
These  pulsations  were  first  thought  by  me  to  be  in  the  carotid 
artery,  but  are  now  known  to  be  jugular. 

My  diagnosis  of  the  cardiac  disease  was  the  same  as  that  of 
others:  aortic  stenosis  of  mild  degree  and  mitral  insuflSciency,  the 
heart  being  in  a  state  of  still-preserved  compensation;  for  although 
vertigo  was  a  symptom,  there  was  no  dyspna?a  on  effort  and  no 
secondary  hepatic  or  other  visceral  engorgement.  Two  things 
greatly  puzzled  me:  first,  if  the  mitral  valve  leaked  why  did  not 
the  obstruction  of  the  aortic  orifice  render  the  regurgitation 
through  the  mitral  more  serious,  as  is  usually  the  effect;  and,  sec- 
ond, what  was  the  cause  of  the  vertigo,  or  rather  the  irregularity, 
in  the  heart's  action. 

This  latter  condition,  I  believed,  was  in  some  manner  connected 
with  his  digestive  organs,  but  just  how  I  could  not  decide.  The 
urine  was  collected  for  twenty-four  hours  and  carefully  examined 
in  the  Columbus  Medical  Laboratory,  but  aside  from  some  con- 


328  DISEASES  OF  THE   HEART 

centration  was  negative.  The  genitalia  were  examined  by  a  com- 
petent specialist,  but  showed  nothing  more  than  slight  urethral 
congestion  and  hyperiesthesia.  The  patient  was  sent  to  an  expert 
neurologist,  who  was  not  able  to  discover  any  canse  in  disorder  of 
the  nervous  system.  Diffusible  stimulants  in  frequent  large  doses 
for  many  hours  were  administered  without  appreciable  effect,  as 
were  cathartics  and  remedies  to  improve  digestion;  all  to  no  pur- 
pose. The  case  was  dismissed,  therefore,  as  an  enigma  and  with- 
out a  parallel  in  my  experience.  It  was  not  at  this  time  recog- 
nised as  an  instance  of  Stokes-Adams  disease. 

But  now  comes  the  still  more  interesting  sequel.  At  Christmas- 
time, 1900,  this  same  young  officer  reappeared  with  the  statement 
that  during  the  previous  summer  he  had  visited  Bad  Nauheim  and 
been  treated  with  baths  by  Dr.  Schott  without  any  benefit;  had 
been  examined  by  a  number  of  competent  men,  among  whom  was 
Rosenbach  of  Berlin,  No  one  had  given  him  any  help,  and  no  one 
had  decided  the  precise  nature  of  his  heart-trouble.  Rosenbach 
indeed  had  diagnosticated  the  aortic  stenosis,  but  was  undecided  as 
to  what  was  the  condition  at  the  mitral.  I  found  things  exactly 
as  a  year  earlier.  But  strong  in  my  belief  that  the  vertigo  that 
still  continued  was  in  some  way  related  to  his  digestion,  or  met- 
abolism, or  excretion,  or  all  together,  I  persuaded  the  young  man 
to  try  for  a  month  an  absolutely  non-animal  dietary,  by  which  was 
meant  the  exclusion  of  anything  derived  from  the  animal  kingdom, 
including  meat,  poultry,  fish,  eggs,  etc.,  with  exception  of  cheese 
and  milk.  These  and  butter,  of  course,  were  to  be  allowed,  to- 
gether with  all  kinds  of  cereals,  vegetables,  fruits,  nuts,  and  breads. 
For  several  weeks  his  urine  was  sent  to  me  for  analysis,  and  was 
always  loaded  with  indican  and  oxalic  acid,  but  in  other  respects 
was  normal.  Nearly  four  months  later  the  patient  reappeared 
Avith  a  perfectly  regular  pulse  of  26,  and  was  entirely  free  from  his 
vertigo,  which  he  stated  had  left  so  soon  as  he  began  the  prescribed 
diet  and  had  not  once  recurred. 

Examination  of  the  heart  showed  the  condition  unchanged  ex- 
cepting regularly  interposed  between  every  two  vigorous  cardiac 
systoles  were  two  feeble  contractions  that  produced  palpable  and 
visible  small  pulsations  in  the  right  common  carotid,  as  well  as 
weak  heart-sounds,  but  no  perceptible  radial  pulse.  The  actual 
heart-rate  was  therefore  78.     The  sul)joined  sphygmographic  tra- 


AORTIC  STENOSIS  329 

cing  (Fig.  65)  was  taken  by  Dr.  Edward  F.  Welles,  and  is  by  him, 
a  competent  judge,  considered  entirely  normal  except  in  rate. 


Fig.  65. — Sphygmogram  fkom  Case  of  Aortic  Stenosis  (p.  324j. 
Pulse-rate,  25  per  minute. 

The  conclusions  to  which  I  am  forced  by  this  case  are  the  fol- 
lowing: 1.  That  this  singular  cardiac  action  is  normal  to  this  in- 
dividual, and  that  it  is  only  its  irregularity  that  occasions  symp- 
toms of  any  kind.  2.  That  this  irregularity  was  of  an  auto-infec- 
tious origin,  due  either  to  the  production  of  leucomaines  or  to  the 
influence  of  constipation  on  the  vagus  or  heart-muscle  cells,  for  on 
this  new  dietary  he  has  had  two  or  more  bowel  movements  daily. 
3.  That  the  lesion  is  a  mild  aortic  stenosis  together  with  a  mitral 
defect,  of  the  exact  nature  of  which  I  am  not  certain.  But  as 
I  feel  sure  that  at  my  last  examination  I  detected  a  very  short 
presystolic  thrill  and  murmur  as  well  as  an  apex-systolic  murmur, 
I  am  inclined  to  the  opinion  that  there  is  both  narrowing  and  re- 
gurgitation at  the  mitral  ostium.  Why  this  combined  lesion  does 
not  occasion  secondary  signs  and  symptoms  can  only  be  explained 
on  the  hypothesis  that  the  defects  are  slighter  than  would  be  sup- 
posed from  the  cardiac  findings,  particularly  the  intensity  of  the 
murmurs.  The  peculiarity  of  his  normal,  or  at  least  seemingly 
normal,  cardiac  action,  is  still  inexplicable.  The  symptoms  in  this 
case  do  not  as  such  belong  to  the  usual  history  of  aortic  stenosis, 
but  are  here  narrated  because  they  may  be  remotely  referred  to 
the  valvular  lesion  and  illustrate  the  vertigo  said  to  be  sometimes 
dependent  upon  narrowing  of  the  aortic  ostium. 

It  is  apparent  that  the  development  of  subjective  symptoms 
is  determined  by  other  conditions  than  the  mere  existence  of  aortic 
stenosis.  They  depend  upon  either  disordered  or  deficient  cardiac 
action.  When  at  length,  either  in  consequence  of  overstrain  or  of 
extreme  narrowing,  the  left  ventricle  begins  to  manifest  inade- 
quacy, dilatation  sets  in,  and  it  is  no  longer  able  to  completely 
23 


330  DISEASES  OP  THE   HEART 

empty  itself.  Symptoms  of  stasis  back  of  the  point  of  constriction 
now  appear.  Left  ventricle  weakness  may  be  shown  by  feebler 
systoles  and  a  more  rapid,  even  irregular  pnlse.  Always  small  and 
of  low  tension,  it  now  becomes  still  emptier,  and  at  the  same  time 
more  rapid  than  formerly. 

When  in  the  course  of  time  dilatation  leads  to  relative  mitral 
insufficiency,  the  clinical  features  become  those  of  mitral  regur- 
gitation in  an  intense  degree.  Even  before  things  have  reached 
this  grade,  however,  the  patient  has  noticed  more  or  less  breath- 
lessness  on  exertion,  and  it  may  be  also  attacks  of  palpi- 
tation. 

If  now  the  heart  is  carefully  percussed,  it  is  found  that  the 
right  ventricle  has  increased  in  size,  while  there  are  in  addition 
signs  of  engorgement  of  the  general  venous  system.  This  condi- 
tion may  last  for  months  before  relative  mitral  insufficiency  be- 
comes pronounced,  but  as  a  rule  the  condition  grows  more  or  less 
rapidly  worse  and  the  individual  is  no  longer  able  to  keep  about 
because  of  dyspnoea  and  congestion.  A  mitral  systolic  murmur  is 
added  to  that  of  the  aortic  stenosis,  the  right  ventricle,  feeling  the 
strain  of  pulmonary  congestion,  begins  to  pulsate  in  the  epigas- 
trium, the  cervical  and  superficial  veins  swell,  the  liver  grows  pal- 
pable and  tender,  the  urine  becomes  scanty  and  concentrated,  and 
at  last  oedema  makes  its  appearance  in  the  feet  and  ankles.  The 
case  has  now  become  converted  into  one  of  mitral  disease  in  the 
stage  of  broken  compensation. 

When  the  mitral  orifice  shares  in  the  dilatation  of  the  ventricle, 
the  ensuing  regurgitation  acts  as  a  safety-valve,  the  same  as  in 
cases  of  aortic  incompetence,  and  actually  serves  to  prolong  life. 
Not  infrequently  the  strain  on  the  right  heart  leads  also  to  rela- 
tive tricuspid  leakage,  and  we  have  the  signs  of  that  lesion  added 
to  those  of  the  aortic  and  mitral  defects.  When  this  state  is  reached 
the  patient's  sufferings  are  often  extreme,  and  may  be  protracted 
through  many  months. 

In  the  spring  of  1898  I  first  took  charge  of  a  lady  of  forty-one 
who  had  an  extreme  and  apparently  pure  stenosis  of  the  aortic 
orifice  of  rheumatic  origin.  Six  years  before,  the  late  Dr.  W.  W. 
.laggard  delivered  her  of  a  son,  and  recognised  the  gravity  of  the 
case  because  of  the  valvular  lesion.  The  lady  did  not  subsequently 
experience  distinctive  cardiac  symptoms  until  the  care  of  a  con- 


AOJlTIC  STENOSIS  331 

sumptive  step-son  compelled  her  to  reside  for  many  months  at  a 
considerable  altitude.  Going  with  him-  first  to  Colorado  Springs 
(6,000  feet),  she  there  suffered  intensely  from  shortness  of  breath, 
so  that  they  were  obliged  to  take  up  their  residence  in  the  Pecos 
Valley  at  a  height  of  about  2,.">00  feet.  Even  there  she  was  not 
able  to  walk  without  considerable  dyspncea. 

After  the  death  of  the  young  man  this  lady  went  abroad,  and 
in  Europe  sought  medical  advice.  She  was  advised  to  take  a  course 
of  baths  under  Dr.  Schott,  at  Bad  Xauheim,  and  while  there  had 
her  first  violent  attack  of  angina  pectoris.  This  folloAved  one  of 
her  baths.  ]^o  special  benefit  was  produced  by  the  balneological 
treatment,  and  she  returned  to  America.  During  the  winter  of 
1897  and  1898  she  passed  through  an  attack  of  acute  nephritis,  but 
wdien  she  consulted  me  the  urine  showed  no  albumin  or  other  ab- 
normal findings.  The  heart  was  greatly  enlarged,  but  compensa- 
tion was  still  fair.  That  summer  she  had  a  violent  attack  of  angina 
following  a  fatiguing  walk  across  a  very  uneven  meadow,  and 
thereafter  was  never  again  well. 

When  I  saw  her  in  the  fall  I  considered  it  necessary  to  confine 
her  to  bed  for  a  number  of  weeks,  and  when  at  length  she  was  per- 
mitted to  get  up  she  was  still  obliged  to  remain  on  one  floor  and  to 
move  about  with  great  slowness.  The  action  of  the  heart  did  not 
quicken  much  under  exertion^  but  the  pulse  grew  very  feeble,  the 
veins  of  the  neck  swelled,  and  she  breathed  with  evident  difficulty. 
She  had  several  severe  anginal  seizures,  which  will  be  described  in 
the  article  on  Angina  Pectoris.  Strength  was  gained  with  great 
slowness,  and  she  was  rarely  free  from  more  or  less  cardiac  distress. 
This  took  the  form  chiefly  of  breathlessness,  distention  of  the  ab- 
domen by  flatus,  and  hepatic  congestion. 

There  was  never  any  oedema,  but  the  ankles  often  felt  swollen 
and  stiff.  She  passed  the  summer  of  1899  at  the  seashore  under 
the  care  of  my  friend,  Dr.  Edward  O.  Otis,  of  Boston,  and  in  the 
autumn  returned  no  worse  but  apparently  no  better  as  regarded 
her  heart.  All  these  months  she  had  been  kept  on  approved  cardiac 
tonics  and  was  frequently  obliged  to  resort  to  hydragogue  cathar- 
tics because  of  the  relief  they  afforded.  The  ensuing  winter  was 
a  hard  one  for  her,  as  she  was  most  of  the  time  confined  to  her 
apartments  in  the  care  of  a  trained  nurse.  This  was  necessary  by 
reason  of  the  possibility  of  an  anginal  paroxysm  and  because  at 


332  DISEASES  OF   THE   HEART 

night  she  would  sometimes  awake  deathly  cold,  in  a  drenching 
sweat,  and  feeling  extremely  faint. 

The  pulse  at  these  times  was  small  and  feeble,  and  the  coun- 
tenance was  blue.  Prompt  stimulation  relieved  her,  but  not  al- 
ways speedily,  for  it  seemed  as  if  absorption  from  the  stomach  was 
slow,  and  hence  resort  was  had  to  hypodermics  of  y^„  of  nitro- 
glycerin, followed  at  once  by  heat  to  the  surface  and  diffusible 
stimulants.  During  that  winter,  and  indeed  I  may  say  most  of  the 
time  for  nearly  three  years,  the  pulse-rate  did  not  vary  much  from 
96,  sinking  as  low  as  90  when  she  was  at  her  best,  and  when  at  her 
worst  rising  to  105.  I  believe  that  on  a  few  occasions  I  noted  a 
few  beats  less  than  90,  usually  regular.  As  a  general  thing  the 
pulse  was  tense,  and  exacerbation  of  symptoms  was  invariably 
preceded  by  a  noticeable  increase  in  its  hardness. 

This  patient  was  much  distressed  by  frightful  dreams,  from 
which  she  awoke  with  a  start  and  a  feeling  of  faintness.  She  was 
also  easily  startled  by  unexpected  noises,  although  she  appeared 
to  have  her  nerves  under  good  control.  Insomnia  was  very  dis- 
tressing, and  yielded  to  nothing  so  well  as  to  hypnotism.  She 
had  to  be  extremely  careful  in  diet,  for  at  times  everything  seemed 
to  create  gaseous  distention  of  the  stomach  and  bowels  with  imme- 
diate aggravation  of  her  dyspnoea.  During  that  winter  relative 
incompetence  of  the  mitral  valve  became  constant,  and  every  now 
and  then  tricuspid  regurgitation  was  added.  Even  without  actual 
leakage  of  the  tricuspid  valve  the  cervical  veins  remained  much 
distended  and  at  times  caused  pain  by  their  pressure.  I  have 
since  noted  painful  swelling  of  the  jugulars  in  another  patient,  but 
as  a  rule  have  not  known  patients  to  complain  of  actual  pain  from 
this  cause. 

Whenever  an  attempt  was  made  to  invigorate  the  circulation 
by  considerable  doses  of  digitalis  or  other  cardiac  tonics,  this  pa- 
tient became  annoyed  by  a  feeling  in  the  heart,  which  she  charac- 
terized as  "  pounding,"  so  that  the  treatment  finally  settled  down 
to  an  attempt  to  keep  down  pulse  tension  and  stasis  by  moans 
of  nitroglycerin  and  cathartics,  with  strychnine  and  caffeine  in 
small  four-hourly  doses,  and  careful  feeding. 

Thus  weeks  dragged  into  months,  spring  came  and  passed,  the 
heated  term  was  at  hand,  with  its  thunder-storms,  for  which  she 
possessed  an  uncontrollable  ])h()bia,  and  she  was  again  sent  down 


AORTIC  STENOSIS  333 

to  Dr.  Otis,  at  Rye  Beach.  B}-  fall  her  condition  grew  so  threat- 
ening from  cardiac  dilatation  and  visceral  congestion  that  she  was 
not  able  to  return  to  Chicago  until  Thanksgiving.  When  at  last 
she  was  able  to  make  the  journey  and  reached  home  I  found  her 
in  a  deplorable  state.  Both  auriculo-ventricular  valves  were  leak- 
ing, and  the  liver  was  enormously  increased  in  size.  The  lungs 
were  so  congested  that  she  was  harassed  by  a  frequent  cough, 
which  completely  exhausted  her,  made  the  face  actually  purple, 
and  caused  her  to  gasp  for  breath  for  many  minutes. 

The  difficult  sputum  was  often  bloody,  or  if  not  actually  san- 
guineous was  made  up  of  thick,  tough  brownish  mucus.  The  bases 
of  the  lungs  were  dull,  and  everywhere  were  copious  moist  and  dry 
rales.  Heroin,  strychnine  hypodermically,  energetic  catharsis, 
and  apomorphine  in  -g-grain  doses  at  last  pulled  her  out  of  her 
desperate  condition,  and  by  Christmas  she  was  reasonably  com- 
fortable. She  was  obliged  to  remain  in  bed,  however,  or  to  ex- 
change this  for  an  invalid's  chair.  A^Tienever  she  made  this  eifort 
her  pulse  grew  weak,  the  veins  distended,  and  she  was  unable  to 
speak  for  a  minute  or  two  on  account  of  shortness  of  breath. 

The  excitement  and  fatigue  of  the  holidays  nearly  used  her  up. 
Her  cough  returned  with  increased  visceral  hypersemia  and  be- 
came so  frequent  and  distressing  that  it  could  only  be  controlled 
by  hypodermic  administration  of  hydrochlorate  of  heroin  -^^  of  a 
grain.  This,  however,  after  a  day  or  two  produced  nausea  and 
vomiting,  and  then  I  actually  feared  the  strain  of  emesis  would 
make  her  heart  stop  beating  altogether.  As  it  was,  after  each 
vomiting  spell  she  sank  back  on  her  pillows,  blue  in  the  face,  gasp- 
ing for  breath  and  too  exhausted  to  speak,  while  the  perspiration 
simply  poured  oif  of  her. 

At  length,  however,  things  mended  somewhat,  and  if  not  rea- 
sonably comfortable,  she  was  at  least  not  miserable.  Then  albu- 
min and  casts  appeared  in  the  urine  in  large  amounts,  and  this 
patient  sufferer  began  to  fail  slowly  but  steadily.  By  the  middle 
of  January  it  became  necessary  to  resort  to  stimulating  injections 
of  morphine  and  atropine  to  keep  off  the  horrible  sensation  of 
fainting  which  took  possession  of  her.  Strychnine  was  increased 
to  the  limit  of  toleration,  and  in  addition  hypodermics  of  a  grain 
of  valerianate  of  caffeine  were  also  given  every  two  hours. 

Stasis  became  so  distressing,  although  oedema  was  never  a  very 


334  DISEASES   OP  THE   HEART 

marked  feature,  that  cathartics  became  a  daily  necessity.  I  recog- 
nised that  the  morphine  was  a  two-edged  sword,  increasing  the 
danger,  of  urannia  and  upsetting  the  stomach,  while  at  the  same 
time  affording  her  relief  from  positive  misery,  and  therefore  it 
was  not  withheld.  At  length,  towards  the  end  of  February,  this 
boon  became  so  necessary  that  more  than  a  grain  a  day  was 
administered.  This  sufferer's  craving  for  stimulation  be- 
came most  urgent  and  distressing — so  much  so  that  whenever 
the  effect  of  the  stimulants  passed  off  she  at  once  felt  a  ter- 
rible sensation  of  dying.  Of  course  this  could  not  be  kept  up 
for  long,  and  finally,  five  days  before  her  death,  the  stomach 
gave  out.  Whether  owing  to  the  morphine,'  to  the  gastric 
hypera?mia,  to  irritation  of  the  nerve-centres,  or  urjcmia,  I  am 
not  able  to  say,  the  vomiting  became  incessant  except  when  she 
was  under  the  influence  of  large  doses  of  morphine,  as  often  as 
every  five  bours. 

There  actually  seemed  to  be  no  circulation  at  times,  as  judged 
by  the  state  of  the  venous  system,  and  yet  that  poor  heart  kept 
right  on,  beating  105  times  a  minute,  and  for  the  most  part  regu- 
larly. It  seemed  as  if  the  end  must  come  at  any  moment  through 
diastolic  arrest  of  the  organ,  and  yet  merciful  death  was  withheld 
for  five  weary  days.  At  length,  forty  hours  before  the  struggle 
ceased,  I  stopped  all  medication,  except  what  morphine  was  actu- 
ally required  to  prevent  unnecessary  suffering,  in  the  hope  that  by 
so  doing  the  end  might  be  hastened.  Still  that  heart  went  on, 
although  gradually  growing  weaker  and  weaker.  Twenty  hours 
prior  to  death  she  sank  into  coma — merciful  coma — and  at  five 
o'clock  in  the  morning  the  sufferer  suddenly  gave  a  little  gasp, 
there  came  a  gush  of  blood  to  her  lips,  and  all  was  over.  Death 
was  probably  due  to  pulmonary  apoplexy,  in  consequence  of 
sudden  nrrest  of  the  left  ventricle  nn  instant  before  that  of  the 
riglit. 

No  excuses  are  offered  for  the  detailed  narration  of  this  case, 
since  I  believe  it  is  highly  instructive.  Two  years  and  a  half 
elapsed  between  the  time  this  patient  first  took  to  her  bed  and  her 
death,  and  during  all  these  thirty  months  it  was  one  uujceasing 
fight  against  the  inevitable.  The  original  defect  at  the  aortic  ori- 
fice became  converted,  so  far  as  symptoms  wore  concerned,  into  a 
mitral  and  tricuspid  regurgitation ;  l)uf  with  this  difference,  that 


AORTIC  STENOSIS  335 

the  aortic  narrowing  absolutely  precluded  all  possibility  of  over- 
coming the  dilatation  of  the  left  ventricle  and  the  closing  of  the 
mitral  valves.  Every  now  and  again  treatment  closed  up  the 
tricuspids,  but  nothing  could  restore  adequate  arterial  circula- 
tion. The  more  one  tries  in  such  cases  to  force  the  left  ventricle 
to  contract  energetically  the  more  is  its  dilatation  likely  to  be 
increased. 

In  this  case  there  was  another  element  that  had  to  be  reckoned 
with — namely,  the  angina  pectoris  and  the  probable  degeneration 
of  the  myocardium  resulting  from  the  cardiac  ischnemia  that  led 
to  the  angina.  From  the  start  I  foresaw  the  inevitable  result,  and 
we  only  put  up  as  good  a  fight  as  we  could. 

Physical  Signs. — Inspection. — In  most  cases  of  aortic  steno- 
sis there  is  nothing  in  the  patient's  appearance  to  attract  attention 
unless  it  be  some  degree  of  pallor.  Cyanosis  is  not  present  so  long 
as  compensation  is  preserved,  and  therefore  when  observed  it  is 
indicative  either  of  some  associated  lesion  or  of  cardiac  inade- 
quacy that  has  led  to  stasis.  The  chief  value  of  inspection  lies  in 
the  fact  that  it  enables  one  to  detect  the  location  of  the  apex-beat. 
This,  in  consequence  of  the  hypertrophy  of  the  left  ventricle,  is 
seen  displaced  downward  and  outward,  the  extent  of  displace- 
ment depending  upon  the  degree  of  hypertrophy.  In  thin 
individuals  with  broad  intercostal  spaces  there  is  sometimes  a 
diffused  lifting  of  that  portion  of  the  chest-wall,  overlying  the 
left  ventricle,  but  this  is  rarely  so  pronounced  as  in  aortic  regur- 
gitation. 

Palpation. — Tlie  hand  laid  upon  the  priecordia  perceives  a 
slow,  broad,  heaving  impulse,  and  at  once  receives  the  impression 
of  a  powerfully  contracting  organ.  Palpation  is  consequently  a 
valuable  means  of  examination  by  enabling  one  to  judge  of  the 
contractile  energy  of  the  left  ventricle.  In  corpulent  persons  the 
thickness  of  the  thoracic  parietes  may  conceal  the  real  force  of 
the  apex-beat,  but  as  a  rule  feebleness  of  the  impact,  even  when 
the  apex  is  displaced,  is  a  token  that  dilatation  of  the  ventricle  is 
weakening  its  systoles.  Furthermore,  in  many  cases  of  aortic 
narrowing  careful  palpation  of  the  base  of  the  heart  detects 
a  thrill  or  fremissement  at  some  point  along  the  course  of  the 
ascending  aorta.  This  is  generally  in  the  second  right  inter- 
space close  to  the  edge  of  the  sternum,  but   it  may  be  on  the 


336 


DISEASES  OF  THE  HEART 


Fig.  66. — Sphtgmogram  of    Uncomplicated 

Aortic  Stenosis. 

Personal  observation. 


breastbone  or  in  the  third  interspace,  immediately  adjoining 
the  left  sternal  border.  The  intensity  of  this  thrill  is  variable, 
bnt  its  rhythm  is  always  systolic.  It  is  needless  to  remind  the 
reader  that  this  vibration  is  the  palpable  expression  of  eddies  or 
currents  in  the  blood-stream  after  it  has  passed  the  point  of  con- 
striction. 

The  pnlse  of  aortic  stenosis  is  small  and  usually  weak  in  con- 
sequence of  the  diminution  in  the  amount  of  blood  ejected  from 
the  ventricle.  Its  size  there-  ^^^^^^^^^^^^^^^^^^^^ 
fore  furnishes  indication      I^^Sl^^SI^^SI^^S^H 

the  So      IHI^K^^IH^^IH^^I^I 

long  as  the  myocardium  is 
healthy  and  compensatory  hy- 
pertrophy is  maintained  the 
pulse  is  regular,  and  in  rate  is  generally  somewhat  below  the  nor- 
mal. Accordingly,  an  undue  acceleration,  or  an  irregularity,  or 
intermittence  of  the  pulse  is  a  sign  of  weakness.  If  aortic  incom- 
petence is  associated  the  pulse  is  likely  to  be  modified  in  accord- 
ance with  the  characters  of  that  lesion.      The   sphygmographic 

tracing  of  aortic  stenosis 
shows  rather  distinctive  char- 
acters. The  amplitude  is  not 
great,  the  line  of  ascent  is 
oblique,  the  summit  rounded, 
the  descent  gradual,  and  the 
secondary  waves  indistinct. 
These  characters  are  shown 
in  Fig.  6G,  Avhich  is  the  copy 
of  a  tracing  obtained  from  one 
of  my  patients  who  presented 
the  signs  of  pure  and  uncom- 
plicated narrowing  of  the 
ostium,  tliere  being  no  dias- 
tolic murmur  of  regurgita- 
tion, and  the  left  ventricle 
hypertro])hied  with  very  little 
dilatation. 

Percussion. — So  long  as  compensation  is  preserved,  deep- 
seated  cardiac  dulness  is  increased  towards  the  left  and  downward 


Fii..  67. — Tvi'ii;al  Kelative  J)ri.NKss  i\ 
Case  of  WEi.L-coMPEXfATEi)  Aortic 
Stenosis. 


AORTIC  STENOSIS 


m 


to  an  extent  commensurate  with  the  degree  of  left  ventricle  hyper- 
trophy (Fig.  67).  It  is  only  when  failing  compensation  has  led 
to  pulmonary  congestion,  or  when  aortic  stenosis  is  united  with  a 


Fig.  68. — Khythm  of  Aortic  Obstructive  Murmur. 


mitral  defect,  that  percussion  detects  any  increase  of  absolute  and 
relative  cardiac  dulness  to  the  right. 

Auscultation. — The  first  sound  at  the  apex  is  apt  to  be 
dull  and  muffled  in  conse- 
quence of  the  preponderance 
of  its  muscular  element,  while 
the  second  tone  is  likely  to  be 
enfeebled.  Over  the  base  of 
the  heart  in  the  aortic  area 
the  ear  perceives  a  murmur 
which  is  synchronous  with  the 
first  sound,  and  is  therefore 
systolic  (Figs.  68  and  69). 
In  pure  stenosis  there  is  only 
this  one  bruit,  but  not  infre- 
quently there  is  also  a  dias- 
tolic murmur  due  to  accom- 
panying   aortic    regurgitation. 

rpi  .    T  T1       j-l,^        Fig.    69. — Place    of    Maximum     Intensity 

1  he  systolic  murmur,  like  the  ,  .  x.       ^  .„  ^ .   ^^ 

"J  '  _  (small    circle)    and    Propagation    of 

thrill,   is   of  variable   intensity,  Aortic  Stenotic  Mu-rmur. 


338  DISEASES  OF   THE   HEART 

but  as  a  rule  it  is  heard  with  great  distinctness,  and  is  of  a 
harsh  or  grating  quality.  Its  direction  of  propagation  is  with 
the  blood-stream  upward  into  the  neck,  and  it  is  not  rare  for  the 
bruit  to  be  audible  in  the  left  interscapular  region  along  the 
course  of  the  descending  aorta.  In  exceptional  instances  when 
very  intense  it  is  heard  throughout  the  praecordia,  particularly 
upon  and  down  the  sternum,  being  sometimes  most  distinct  in  the 
left  third  interspace  over  the  anatomic  seat  of  the  aortic  valves. 
The  murmur  generally  replaces  the  first  tone  at  the  base,  and  when 
the  valves  are  too  stiff  and  thick  to  close,  the  second  tone  in  the 
aortic  area  and  in  the  cervical  arteries  is  wanting  or  so  enfeebled 
as  to  be  merely  a  rudimentary  click.  Consequently,  in  those  cases 
in  which  the  aortic  second  sound  is  retained  in  its  normal  intensity 
and  clearness,  this  fact  suggests  the  possibility  that  the  obstruc- 
tion is  situated  in  the  conus  arteriosus  or  at  the  ostium,  the  valves 
themselves  lieing  but  slightly  affected. 

Diagnosis. — As  a  general  thing  there  is  but  little  difficulty  in 
diagnosticating  the  disease  in  question.  The  conjunction  of  signs 
of  left  ventricle  hypertrophy  with  a  systolic  murmur  in  the  aortic 
area  and  enfeeblemcnt  of  the  second  tone  at  the  right  of  the  ster- 
num, is  as  a  rule  sufficient  evidence  for  its  diagnosis,  particularly 
if  the  person  is  under  forty,  and  furnishes  a  history  of  a  previous 
attack  of  rheumatism.  There  are  three  conditions,  however,  that 
must  be  differentiated :  (1)  sclerosis  of  the  aorta  or  its  valves  with- 
out obstruction,  (2)  aortic  aneurysm,  and  (3)  an  accidental  mur- 
mur, often  called  anamiic. 

In  favour  of  arteriosclerosis  are  the  following:  ^Middle  or  ad- 
vanced age,  stiffened  peripheral  arteries,  accentuation  and  ringing 
quality  of  the  aortic  second  sound.  The  left  ventricle  alone  may 
be  hypertrophied,  but  in  most  cases  the  whole  heart  is  enlarged. 
A  history  of  syphilis  as  against  inflammatory  rheumatism  also 
makes  strongly  for  sclerosis  instead  of  stenosis.  The  difficulty  is 
still  further  increased  by  the  consideration  that  degenerative 
changes  may  lead  to  narrowing  of  the  orifice  in  one  way  or  an- 
other. Consequently,  a  precise  differential  diagnosis  between 
these  two  diseases  cannot  always  l)e  made. 

As  regards  an  aortic  aneurysm — every  one  knows  that  when 
this  is  small  it  is  often  impossilile  of  detection,  yet  the  following 
differential  points  may  be  stated :  The  patient's  age,  being  forty 


AORTIC  STENOSIS  339 

or  more,  a  history  of  syphilis  or  of  injury  or  strain,  stiff  arteries, 
symptoms  of  pressure,  as  pain,  dyspnoea,-  and  cough,  inequality  in 
the  size  of  the  pulses  of  the  neck  and  upper  extremities,  displace- 
ment rather  than  hypertrophy  of  the  heart,  pulsation,  particularly 
if  expansile  and  combined  with  bulging  in  the  aortic  area,  circum- 
scribed dulness  over  the  manubrium  sterni  or  at  either  side,  and 
in  addition  to  the  systolic  aortic  murmur,  a  booming  second  tone 
that  is  not  quite  pure  or  is  accompanied  by  a  faint  bruit.  If 
doubt  is  still  entertained,  resort  should  always  be  had  to  the  X- 
ray.  Indeed,  if  this  means  of  diagnosis  is  accessible,  it  should  be 
appealed  to  for  confirmation  in  all  cases.  Mediastinal  tumours 
pressing  on  the  aorta  are  so  rare  that  they  will  not  be  considered. 

If  all  the  signs  of  aneurysm  just  mentioned  were  present  in 
every  case  a  differential  diagnosis  would  not  be  difficult,  but  un- 
fortunately such  is  seldom  the  case.  I  recall  a  patient  in  the 
wards  of  Cook  County  Hospital  who  presented  a  conjunction  of 
signs  that  rendered  the  condition  of  his  aortic  orifice  a  subject  of 
much  controversy,  and  owing  to  his  departure  from  the  hospital 
were  never  cleared  up.  In  this  case  there  was  a  history  of  syn- 
copal attacks,  and  this  fact,  it  was  argued  by  some,  made  strongly 
for  stenosis.  On  the  other  hand,  I  felt  quite  certain  of  a  circum- 
scribed area  of  deep-seated  dulness  in  the  first  interspace  close  to 
the  right  sternal  margin,  and  therefore  believed  the  condition  was 
more  likely  an  aneurysm. 

Lastly,  an  accidental  murmur  in  the  aortic  area  may,  when 
occurring  in  the  young,  give  rise  to  the  suspicion  of  a  stenosis. 
The  error  can  be  avoided  by  attention  to  the  following  points :  The 
absence,  it  may  be,  of  a  rheumatic  history,  the  sex  (the  patient 
being  most  frequently  a  female,  in  whom  aortic  stenosis  is  compara- 
tively rare),  the  absence  of  left  ventricle  hypertrophy,  retention 
of  the  aortic  second  sound,  the  presence  of  other  accidental  mur- 
murs in  other  areas,  as  pulmonary  and  mitral,  the  softer  quality 
of  the  murmur,  greater  frequency  of  the  radial  pulse,  and  the 
detection  of  ana?mia  in  some  instances. 

Prognosis. — This  depends  upon  the  etiology  of  the  affection 
and  the  degree  of  compensation  that  has  been  established.  If  ste- 
nosis has  resulted  from  degenerative  changes  in  the  valves,  there 
are  likely  to  be  associated  defects  in  the  aortic  walls,  and  it  may 
be  in  the  coronary  arteries,  which  seriously  affect  the  blood-supply 


340  DISEASES  OF  THE  HEART 

to  the  heart,  and  hence  prognosis  is  correspondingly  unfavourable. 
Under  such  conditions  compensatory  hypertrophy  cannot  be  main- 
tained for  long,  even  if  it  has  been  developed.  For  the  same  rea- 
son there  can  be  but  slight  hope  of  its  reinstatement  after  it  has 
once  shown  indications  of  breaking.  In  these  unpromising  cases 
the  assurance  cannot  safely  be  given  that  sudden  death  will  not 
take  place.  In  this  respect  it  presents  a  similarity  to  aortic  regur- 
gitation. 

When  the  stenosis  has  been  produced  by  endocarditis  in  the 
young,  the  life-prospect  stands  in  direct  relation  to  the  degree  of 
narrowing  and  the  perfection  of  compensation.  Cases  of  moderate 
severity  may  exist  many  years  without  symptoms,  and  the  patient 
may  be  likely  to  die  of  some  intercurrent  disease.  This  is  substan- 
tiated by  the  frequency  with  which  aortic  obstruction  is  discov- 
ered post  mortem  in  cases  in  which  its  existence  was  not  known  or 
in  nowise  contributed  to  the  individual's  death. 

When,  however,  compensation  has  once  begun  to  break  down, 
even  though  the  heart-muscle  is  not  greatly  degenerated,  the  prog- 
nosis becomes  most  serious.  The  loss  of  compensation  is  due  to 
initiation  or  increase  of  dilatation  in  consequence  of  the  resistance 
having  become  disproportionate  to  the  strength  of  the  ventricle. 
In  most  instances,  to  be  sure,  the  myocardium  of  the  ventricle  has 
suffered  degeneration  of  its  contractile  elements,  in  consequence  of 
the  small  supply  of  blood  sent  to  the  coronary  arteries;  yet  by 
reason  of  the  progressive  nature  of  the  valvular  defect  the  ostium 
may  at  length  become  so  reduced  in  size  that  even  a  healthy  ven- 
tricular wall  cannot  carry  on  adequate  coronary  circulation.  In 
either  contingency  it  is  out  of  the  question  for  the  ventricle  to 
again  develop  predominating  and  adequate  hypertrophy.  Accord- 
ingly, the  prognosis  is  very  different  from  that  of  failing  compen- 
sation in  mitral  regurgitation,  in  which,  if  not  too  badly  lost,  it 
may  be  repeatedly  restored. 

Mode  and  Causes  of  Death. — Stenosis  of  the  aortic  ori- 
fice randy  LennuuUes  in  Hudden  death.  Certainly  it  possesses  no 
inherent  tendency  to  such  an  end,  as  aortic  regurgitation  may  be 
said  to  possess.  In  obstruction  tlio  failing  ventricle  tends  to  grad- 
ual, not  sudden  dilatation,  and  hence  the  fatal  issue  is  likely  to 
come  through  the  effects  of  progressing  stasis,  the  same  as  in 
mitral  defects.     In  some  cases  increasing  weakness  of  the  heart 


AORTIC  STENOSIS  341 

ends  in  fatal  exhaustion  before  oedema  and  transudation  into  the 
serous  cavities  become  marked.  The  last -weeks,  or  even  months, 
of  life  may  accordingly  be  highly  distressing  to  both  patient  and 
friends,  and  death  be  welcomed  as  a  deliverer. 

Of  20  cases  of  aortic  stenosis  Hustedt  found  the  following 
causes  of  death :  Cardiac  asthenia  2,  pulmonary  phthisis  7,  pneu- 
monia 3,  marasmus  2,  pulmonary  oedema,  apoplexy,  nephritis, 
bronchitis,  emphysema,  carcinoma,  and  ana?mia,  each  1.  It  is 
noteworthy  that  but  2,  or  0.9  per  cent,  were  attributable  directly 
to  the  heart,  while  the  remaining  20  were  due  to  intercurrent  dis- 
eases. It  is  also  interesting  to  note  that  in  7  cases  death  was  due 
to  pulmonary  tuberculosis,  and  that  therefore  aortic  stenosis  may 
be  said  to  predispose  to  this  disease,  probably  in  consequence  of 
the  general  malnutrition,  which  is  favoured  by  obstruction  at  the 
aortic  orifice.  This  finds  further  corroboration  in  the  fact  that 
2  died  of  marasmus  and  1  of  anaemia. 


342 


DISEASES  OF  THE  HEART 


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CHAPTER   X 
TRICUSPID    REGURGITATION 

This  is  the  most  frequent  of  the  valvular  lesions  which  affect 
the  right  heart.  It  is  divisible  into  three  classes:  1.  Structural. 
2.  Relative.  3.  Muscular.  Bv  the  last  two  is  meant  incompe- 
tence of  the  valve  clue  either  to  stretching  of  the  ventricle  or  to 
incomplete  coaptation  of  the  cusps  from  defective  contraction  of 
the  ring  or  papillary  muscles. 

Organic  disease  of  these  valves  is  one  of  the  rarer  cardiac  de- 
fects, and  when  found  as  a  chronic  affection  is  generally  congeni- 
tal. It  is  not  as  a  clinical  entity  that  tricuspid  insufficiency  is 
rare ;  it  is  only  the  structural  deformity  of  inflammatory  or  scle- 
rotic nature  that  is  rare.  Concerning  the  frequency  of  relative  tri- 
cuspid regurgitation  Gibson  says :  "  It  is  incomparably  the  most 
common  of  valvular  lesions,  and  that  the  reason  this  fact  is  not 
brought  out  in  statistics  upon  the  relative  frequency  of  valve  de- 
fects is  to  be  found  in  the  circumstance  that  incompetence  of  the 
tricuspid  valve  does  not  in  itself  seriously  impair  the  general 
course  of  the  circulation,  and  it  is  therefore  often  found  among 
those  who,  although  under  treatment  for  various  affections,  have 
no  cardiac  symptoms.  It  accordingly  escapes  observation  unless 
especially  sought  for." 

This  is  a  remarkable  statement,  and  is  at  wide  variance  with 
the  opinion  generally  entertained.  It  would  seem  a  piece  of 
temerity  for  me  to  take  issue  with  Gibson  on  this  point,  but  as  I 
am  not  willing  to  accept  the  presence  of  a  systolic  whiff  in  the 
tricuspid  area  as  conclusive  evidence  of  leakage  at  this  orifice,  I 
must  conclude  that  I  have  overlooked  this  regurgitation  many 
times  when  he  would  have  diagnosed  it.  Doubtless,  in  conse- 
quence of  the  readiness  with  which  the  safety-valve  action  of  this 
incompetence  is  brought  into  play,  there  may  many  times  be  slight 
leaks  that  are  not  considerable  enough  to  produce  positive  venous 
pulse  in  the  cervical  veins  and  liver;   but  this  is  a  matter  of  con- 

343 


344  DISEASES  OF  THE   HEART 

jecture  rather  than  of  demonstration,  and  one  might  argue  that 
the  murmur  is  due  to  some  other  condition  than  actual  regurgi- 
tation. 

Morbid  Anatomy.  ^The  changes  discovered  at  the  tricuspid 
orifice,  whether  they  constitute  a  structural  or  a  relative  defect, 
are  analogous  to  those  at  the  mitral,  and  therefore  a  detailed  de- 
scription of  them  is  omitted.  In  most  cases  in  which  the  incom- 
petence is  owing  to  defects  in  the  valve  itself  there  is  a  comhina- 
tion  of  both  regurgitation  and  obstruction.  Consequently,  more 
will  be  said  on  this  subject  under  the  head  of  Tricuspid  Stenosis. 
When  organic  changes  at  this  ostium  are  encountered,  they  are 
usually  associated  with  lesions  at  other  orifice^,  chiefly  the  mitral. 

When  the  valves  in  question  are  relatively  insufficient  the  right 
ventricle  is  found  dilated  and  its  wall  thin.  The  trabecular  are 
apt  to  show  evidence  of  hypertrophy,  the  papillary  muscles  of 
having  been  stretched,  and  the  valve-flaps  are  often  longer  and 
broader  than  normal,  in  consequence  of  the  prolonged  pressure  to 
which  they  have  been  subjected.  The  auriculo-ventricular  ring  is 
also  stretched,  admitting  more  than  four  fingers.  The  right  auricle 
is  dilated,  in  some  instances  to  an  enormous  extent,  and  its  nor- 
mally thin  wall  is  still  thinner.  It  is  not  uncommon  also  to  find 
that  the  distending  force  of  the  regurgitant  stream  has  induced 
more  or  less  dilatation  of  the  great  venous  trunks  close  to  their 
termination  in  the  auricle. 

The  myocardium  of  the  ventricle  and  auricle  generally  fur- 
nishes evidence  of  prolonged  stasis  in  the  coronary  veins,  or  of 
degeneration.  Finally,  there  are  the  associated  changes  in  the 
lungs  or  left  heart,  which  have  served  as  the  etiological  factors  in 
the  development  of  the  right  ventricle  dilatation  and  eventual  in- 
comi:)etence  of  the  valve. 

Tricuspid  regurgitation  is  a  pathological  condition,  and  yet 
Adams,  and  later  Wilkinson  King,  have  pointed  out  that  it  really 
exerts  a  "  safety-valve  action."  It  occurs  with  remarkable  ease, 
and  these  authors  claim  it  is  a  beneficent  provision  on  the  part  of 
Xatnre  by  whicli  the  heart  is  spared  from  disastrous  overstrain. 
In  the  chapter  on  Aortic  Regurgitation  I  pointed  out  that  relative 
incomiictence  of  the  bicuspid  valve  acts  in  the  same  way.  But 
whereas  the  firmness  of  the  mitral  ring  renders  its  stretching  a 
nuitter  of  mucli  dillicnlty,  tlie  tricuspid  orifice  yields  to  relatively 


TRICUSPID  REGURGITATION  345 

slight  pressure  and  closes  down  again  so  soon  as  the  strain  is  re- 
moved. Consequently,  as  every  clinician  knows,  leakage  through 
the  right  auriculo-ventricular  valve  will  come  and  go  many  times 
in  the  course  of  any  disease  that  throws  excessive  strain  on  the 
right  ventricle. 

Etiology. — Structural  defects  at  the  tricuspid  orifice  are 
generally  produced  during  fcetal  life,  and  are  the  result  of  endo- 
carditis. Nevertheless  these  valves  may  be  the  seat  of  an  inflam- 
matory process  after  birth,  as  well  as,  although  but  seldom,  of 
sclerotic  changes,  the  same  as  other  valves.  When  endocarditis 
attacks  the  right  heart  it  is  usually  associated  with  inflammation 
elsewhere  in  the  heart,  at  one  of  the  other  orifices,  and  owes  its 
origin  to  the  same  etiological  factors,  which  do  not  require  re- 
capitulation here. 

I  shall  therefore  pass  on  at  once  to  the  consideration  of  those 
diseases  and  conditions  that  are  responsible  for  the  causation  of 
the  relative  form. 

Comprehensively  stated,  these  are  all  those  conditions  which 
raise  blood-pressure  in  the  pulmonary  system  to  such  a  point  that 
the  right  ventricle  is  no  longer  capable  of  successful  resistance. 
Occasionally  this  pressure  becomes  so  high  as  to  lead  to  relative 
incompetence  of  the  pulmonary  valves  also,  but  in  most  cases  the 
ring  into  which  they  are  inserted  proves  equal  to  the  strain,  so  that 
it  is  the  ventricular  wall  and  basal  ring  of  the  tricuspid  valve  which 
give  way.  This  degree  of  abnormal  blood-pressure  is  most  fre- 
quently presented  in  mitral  disease,  particularly  stenosis,  and 
hence  it  is  in  these  cases  when  compensation  is  wholly  destroyed 
that  relative  tricuspid  regurgitation  is  most  frequently  recognised. 
Oftentimes  it  follows  the  mitral  incompetence  secondary  to  dilata- 
tion of  the  left  ventricle  in  cases  of  aortic  valvular  disease,  and  it 
is  very  frequently  seen  in  the  terminal  stag^  of  chronic  nephritis. 

In  renal  cirrhosis,  in  particular,  blood-pressure  is  high  and 
sustained,  throwing  great  strain  on  the  left  ventricle.  In  time 
this  chamber,  because  of  degeneration  or  of  the  excessive  periph- 
eral resistance,  begins  to  yield,  dilatation  supersedes  the  hypertro- 
phy, undue  pressure  is  thrown  back  upon  the  right  heart,  and 
the  tricuspid  begins  to  leak.  Thus,  whatever  is  the  nature  of  the 
primary  cardiac  disease,  the  ultimate  effect  is  the  same — namely, 
augmentation  of  blood-pressure  in  the  pulmonic  vessels  and  right 
24 


346  DISEASES  OF  THE  HEART 

ventricle  until  a  point  is  reached  at  which  the  wall  of  the  ventricle 
must  stretch  and   the   valve   become  incompetent. 

Other  diseases  that  produce  the  same  effect  are  vesicular  em- 
physema with  or  without  chronic  bronchitis,  long-standing  bron- 
chial asthma,  cirrhosis  uf  the  whole  or  even  of  a  part  of  one  lung,, 
fibroid  phthisis,  and  pulmonary  collapse  in  consequence  of  pleu- 
ritic effusion.  A  hydrothorax,  itself  consecutive  to  inadequacy  of 
the  heart,  may  by  compression  of  the  lung  hasten  or  intensify  the 
effect  on  the  right  ventricle  of -primary  disease  of  the  left  heart. 
N^o  doubt  in  some  of  the  pulmonary  affections  the  strain  on  the 
right  ventricle  is  intensitied  by  frequent  and  severe  fits  of  cough- 
ing. It  is  probably  in  this  way  largely  that  tricuspid  regurgita- 
tion is  produced  in  cases  of  chronic  bronchitis,  although  many 
times  there  is  an  associated  emphysema. 

The  wall  of  tlie  right  ventricle  is  thinner  than  that  of  the  left, 
and  one  can  readily  understand  that  less  internal  pressure  is  re- 
quired to  bring  about  overdilatation  and  relative  tricuspid  incom- 
petence ;  and  yet  I  cannot  refrain  from  expressing  wonder  at  what 
Gibson  says  concerning  the  influence  of  fever  and  other  conditions 
in  the  production  of  this  valvular  insufficiency.  "  Pyrexia,  if  of 
more  than  brief  duration,  almost  invariably  leads  to  dilatation  of 
the  right  ventricle  and  tricuspid  regurgitation.  It  does  so  some- 
times from  simple  relaxation  of  the  muscular  substance,  but  in 
other  cases  by  means  of  hyaline  degeneration.  Toxic  influences 
belonging  to  almost  every  class  produce  the  same  effect ;  the  tox- 
ines  produced  by  micro-organisms  (sometimes  in  the  absence  of 
all  pyrexia),  the  organic  poisons,  such  as  alcohol,  the  inorganic 
poisons,  such  as  lead,  act  in  precisely  analogous  fashion.  Mal- 
nutrition, wliether  arising  from  some  morbid  process,  as  malignant 
invasion,  from  deficient  absorption,  as  in  such  a  simple  affection 
as  dilatation  of  the  stomach,  or  from  some  deficiency  of  the  food,, 
all  lead  to  the  same  end.  A  long  experience  of  out-patient  service 
in  our  great  hospitals  enables  me  to  bear  M'itness  to  the  extreme 
fre(piency  of  tricuspid  regurgitation  in  atonic  conditions  of  the 
stomach.  Such  disorders  as  anaemia,  in  which  the  nutritive  power 
of  the  blood  is  lowered,  are  also  to  be  considered  as  potent  causes 
of  tricuspid  regurgitation." 

Severe  muscular  exertion,  as  mountain-climbing,  may  and  not 
infrccjuently  does  produce  dilatation  of  the  right  ventricle  and  the 


TRICUSPID   REGURGITATION  347 

safety-valve  action  of  tricuspid  incompetence.  In  such  instances 
the  protective  action  of  this  leak  comes'-beantifully  into  play,  for 
(lid  the  valve  not  give  way  and  allow  the  strain  to  fall  on  the  right 
auricle,  great  veins,  and  liver,  the  continuance  of  the  exertion 
would  eventually  lead  to  dangerous  hnemoptysis  or  fatal  cardiac 
syncope  from  overdistention  of  the  ventricles. 

I  have  within  the  past  twelve  months  seen  two  stalwart  foot- 
ball players  who,  judging  from  the  history  and  the  subsequent 
condition  in  which  I  found  their  right  heart,  must  have  gotten  up 
tricuspid  regurgitation  during  a  game.  In  both,  the  ventricle  and 
cervical  veins  still  showed  permanent  ill  effect  of  their  violent 
exertions.  So  long  as  the  myocardium  of  robust  young  men  is 
healthy,  ultimate  recovery  is  the  rule ;  but  when  after  middle  age 
myocardial  degeneration  exists,  individuals  should  beware  of 
physical  efforts  that  are  likely  to  so  seriously  overstrain  their 
hearts. 

Symptoms. — As  a  matter  of  fact  tricuspid  regurgitation 
exists  so  rarely  alone — that  is,  independently  of  some  other  car- 
diac or  pulmonary  disease — that  our  knowledge  of  its  symptoma- 
tology is  in  reality  derived  from  our  observation  of  the  effects  it 
produces  in  conjunction  with  such  disorders,  or  with  tricuspid 
stenosis.  Nevertheless,  it  would  not  be  difficult  to  deduce  the 
symptoms  from  our  knowledge  of  the  influence  of  this  affection  on 
the  circulation. 

The  first  effect  of  the  regurgitation  is  to  hinder  the  free  flow 
of  blood  out  of  the  right  auricle,  and  thus  bring  about  its  dilata- 
tion. This  reacts  upon  the  contents  of  the  two  vense  cava?,  raising 
pressure  within  them  from  a  negative  to  a  positive  one.  As  nega- 
tive blood-pressure  within  these  two  great  venous  trunks  is  neces- 
sary to  the  maintenance  of  the  circulation,  a  rise  of  blood-pressure 
within  them  and  their  tributary  veins  tends  to  bring  the  blood- 
stream to  a  standstill.  Stasis  thus  induced  shows  itself  by  cyano- 
sis and  turgescence  of  the  superficial  veins  of  the  upper  and  lower 
extremities  and  by  passive  engorgement  of  the  abdominal  viscera. 
The  liver  grows  large  and  tense,  even  to  the  extent  of  tenderness 
and  pain,  particularly  in  the  epigastrium.  Fimctional  visceral 
disorders  in  various  form  show  themselves,  the  feet  and  ankles 
swell  and  ultimately  become  cedematous. 

The  patient  is  weak  and  easily  fatigued,  and  after  a  time  is 


348  DISEASES  OF   THE   HEART 

obliged  to  keep  to  his  room  or  even  to  his  bed.  Dropsy  increases, 
and  may  invade  the  entire  body,  or  ascites  and  hydrothorax  may 
predominate  over  the  anasarca.  Indeed,  Gibson,  who  appears  to 
have  had  a  remarkably  rich  experience  in  this  class  of  cases,  says : 
'^  The  fact  nmst  never  be  overlooked  that  right-sided  disturbances 
are  more  likely  to  produce  interference  with  the  functions  of  the 
pleura  than  affections  confined  to  the  left  side  of  the  heart,  inas- 
much as  the  blood  circulating  in  the  pleural  membrane  is  in  over- 
whelming proportion  returned  to  the  heart  by  the  bronchial  veins, 
w'hich  discharge  their  contents  on  the  right  side  by  means  of  the 
vena  azygos,  and  on  the  left  side  by  means  of  the  superior  inter- 
costal veins.  Their  destination  is  therefore  the  right  auricle. 
When  disturbance  of  the  function  of  the  right  heart  occurs,  there 
is  as  a  consequence  considerable  liability  to  backward  pressure 
upon  the  pleural  membrane,  resulting  in  hydrothorax." 

If  the  tricuspid  regurgitation  is  not  secondary  to  heart  or  lung 
disease,  dyspnopa  and  cough  are  likely  to  come  on  only  after  the 
growing  stasis  in  the  venous  system  has,  through  its  effect  on  the 
general  capillary  and  arterial  circulation,  led  to  pulmonary  con- 
gestion. In  most  cases,  however,  these  symptoms  are  complained 
of  prior  to  the  development  of  the  tricuspid  leakage,  because  form- 
ing a  part  of  the  symptomatology  of  those  diseases  to  which  the 
tricuspid  defect  is  usually  secondary.  Therefore,  as  a  matter  of 
fact,  the  symptomatology  of  this  affection  is  inseparably  linked 
with  that  of  the  antecedent  disorders,  and  does  not  require  recapit- 
ulation. According  to  Gibson,  it  is  possible  for  tricuspid  regurgi- 
tation to  exist  without  producing  any  symptoms,  and  this  is  one 
of  the  reasons  why  it  is  so  frequently  overlooked.  For  my  part 
I  cannot  see  how  this  can  well  be,  and  I  am  not  convinced  by  his 
statement,  for  although  tricuspid  insufficiency  may  not  produce 
cardiac  symptoms,  strictly  speaking,  such  as  dyspnopa  on  exertion, 
still  it  cannot  fail  to  exert  decided  effect  on  the  venous  circulation 
in  general,  which  would  be  sufficiently  serious  to  bring  the  patient 
to  a  physician. 

When  this  valvular  incompetence  arises  in  consequence  of  long- 
standing heart  oi-  lung  disease,  it  speedily  aggravates  the  pre-exist- 
ing symptoms.  The  rapid  a|)pearance  of  general  dropsy  which 
usually  follows  the  establishment  of  regurgitation  is  due  in  large 
part  no  doubt  to  interference  with  the  lymphatic  circulation.     The 


TRICUSPID  REGURGITATION  349 

great  veins  into  whose  blood-stream  the  contents  of  the  thoracic 
duct  are  emjitied  are  so  turgid  that  the  stasis  retards  the  ready 
emptying  of  the  duct.  Congestion  results,  therefore,  in  the  duct 
and  its  tributaries,  injuriously  affecting  nutrition  and  increasing 
the  permeability  of  the  capillary  walls.  This  disturbance  of  the 
circulation  inevitably  results  from  primary  tricuspid  regurgita- 
tion, and  hence  I  cannot  conceive  of  the  disease  remaining  latent. 

Physical  Signs. — Inspection. — Contrary  to  what  is  usually 
the  case  in  diseases  of  the  heart,  inspection  and  palpation  afford 
the  most,  and  according  to  some  the  only,  reliable  means  of  diag- 
nosis in  tricuspid  regurgitation.  This  is  partly  due  to  association 
of  this  lesion  with  other  cardiac  or  pulmonary  diseases  that  pro- 
duce conflicting  physical  signs,  and  partly  to  close  anatomical  con- 
nection between  the  right  chambers  of  the  heart  and  the  great 
venous  trunks,  in  consequence  of  wdiich  the  contents  of  the  latter 
are  directly  exposed  to  pressure  by  the  reflux  stream  in  the  manner 
already  described.  Instead  of  the  large  veins  which  enter  the 
thorax  being  invisible,  the  dilatation  of  the  right  heart  leads  to 
their  permanent  turgescence,  and  in  extreme  degrees  even  to  dila- 
tation of  the  venous  bulbs  at  the  root  of  the  neck.  This  turgidity 
is  specially  marked,  therefore,  in  the  jugulars,  which  may  stand 
forth  like  great  purple  cords. 

When  incompetence  of  the  tricuspid  valve  permits  the  ven- 
tricular systole  to  drive  part  of  its  blood  back  into  the  auricle,  a 
nearly  synchronous  wave  is  transmitted  upward  into  the  veins  of 
the  neck  through  the  superior  vena  cava  and  downward  through 
the  inferior  vena  cava,  even  to  the  liver  or  beyond.  This  reflux 
venous  wave  declares  itself  in  the  neck  as  a  visible  and  even  pal- 
pable pulsation.  This  is  particularly  pronounced  in  the  right  in- 
ternal or  external  jugular,  or  in  both.  This  phenomenon  has  been 
carefully  investigated  by  Riegel,  and  by  him  shown  to  coincide 
with  pulsation  in  the  arteries,  as  the  carotids.  This  "  positive 
venous  pulse,"  as  Riegel  calls  it,  is  usually  spoken  of  as  systolic, 
but  is,  strictly  speaking,  presystolic-systolic,  and  may  be  correctly 
timed  by  comparison  with  the  carotid  pulse.  Simultaneous  paljia- 
tion  of  the  artery  and  inspection  of  the  vein  will  show"  that  pulsa- 
tion in  the  latter  takes  place  during  the  rise  of  the  arterial  pulse. 

In  cases  in  which  there  is  dilatation  of  the  auricle,  yet  without 
tricuspid  regurgitation^  a  venous  pulsation  may  likewise  be  de- 


350  DISEASES  OP  THE  HEART 

tected,  but  its  rhythm  agrees  with  the  hist  portion  of  ventricular 
diastole,  including,  of  course,  auricular  systole,  and  hence  is, 
strictly  speaking,  diastolic-presystolic.  This  venous  pulsation 
occurs,  therefore,  during  the  collapse  of  the  carotid  artery.  This 
diastolic-presystolic  or  "  negative  venous  pulse,"  as  it  is  called, 
never  indicates  tricuspid  insufficiency. 

The  positive  jugular  pulse  of  tricuspid  incompetence  must  also 
be  distinguished  from  a  pulsation  sometimes  communicated  to  the 
distended  vein  from  the  adjacent  artery.  This  can  be  done  by 
pushing  the  artery  away  from  the  contiguous  vein  in  the  case  of 
the  internal  jugular.  To  test  the  external  jugular  it  should  be 
compressed  by  the  finger  a  short  distance  above  the  clavicle,  when, 
if  the  pulsation  is  communicated  from  an  adjacent  artery,  the 
part  below  the  point  of  constriction  will  entirely  or  partially  col- 
lapse and  the  pulsation  disappear  wholly  or  in  part. 

Palpation. — The  corresponding  positive  venous  pulse  con- 
ducted downward  to  the  liver  is  to  be  detected  by  palpation  of  the 
organ.  If  the  congested  liver  is  grasped  by  the  two  hands,  the  left 
pressing  it  strongly  upward  from  behind  and  the  right  being  out- 
spread upon  the  organ  in  front,  pulsation  of  the  liver  is  perceived 
as  an  expansile  distention  in  all  directions.  This  positive  venous 
pulse  in  the  liver  is  therefore  quite  unlike  the  merely  rising  and 
falling  motion  imparted  to  it  by  the  pulsations  of  the  abdominal 
aorta  or  the  downward  impulse  of  the  hypertrophied  right  ventri- 
cle above. 

This  positive  venous  pulse  is  the  pathc^gnomonic  sign  of  tri- 
cuspid regurgitation.  Without  it,  in  either  the  cervical  veins  or 
the  liver,  a  diagnosis  of  this  valvular  lesion  is  ahvays  open  to 
doubt.  There  are  two  exceptions,  ])ut  these  occur  so  rarely  that 
they  seldom  need  to  be  considered.  One  is  a  wave  communicated 
by  the  mitral  regurgitant  stream  through  an  open  foramen  ovale 
to  the  contents  of  the  right  auricle,  and  thus  to  the  stream  in  the 
jugulars.  The  other  is  a  systolic  pulsation  in  the  jugular  veins 
due  to  the  rupture  of  an  aortic  aneurysm  into  the  vein,  instances 
of  which  accident  may  be  found  in  the  literature. 

The  radial  pulse  presents  nothing  distinctive  even  in  primary 
tricuspid  inconi])otonce  without  other  cardiac  disease.  It  is  small 
and  weak,  accelerated  and  regular,  or  irregular  and  intermittent,  as 
the  case  may  be.    Popoff  has  reported  diminution  in  the  size  of  the 


TRICUSPID  REGURGITATION 


551 


right  radial  as  compared  with  the  left,  and  attributed  it  to  pres- 
sure of  the  distended  right  auricle  and  veins  upon  the  right  sub- 
clavian artery. 

Dropsy  is  usually  present  in  cases  of  relative  insufficiency  of 
the  tricuspid  valve,  in  most  instances  following  the  giving  way  of 
the  valve.  It  is  not  present,  however,  in  all  cases,  certainly  in  the 
early  stage  of  the  tricuspid  leakage.  Consequently  this  absence 
of  cutaneous  oedema,  notwithstanding  gTeat  venous  stasis,  is  a 
proof  that  something  more  than  stasis  alone  is  necessary  for  the 
production  of  dropsy.  This  additional  factor  is,  as  previously 
stated,  an  abnormal  permeability  of  the  capillary  walls  or  a  reten- 
tion of  sodium  chloride. 

Percussion. — This  yields  information  of  minor  diagnostic  im- 
portance, because  any  alteration  discovered  in  the  area  of  cardiac 
dulness  may  be  due  to  an  associated  or  antecedent  cardiac  or  pul- 
monary affection.  Vesicular  emphysema,  chronic  pleuritic  effu- 
sion or  hydrothorax,  and  cirrhosis  of  the  right  lung,  may  render 
unavailing  any  attempt  to  determine  by  percussion  the  accurate 
size  of  the  right  heart.  In  vesicular  emphysema  the  borders  of 
the  lungs  are  distended,  pushing  the  heart  away  from  the  chest- 
wall  and  occasioning  such  a 
■degree  of  hyperresonance  that 
the  limits  of  deep-seated  car- 
diac dulness  become  inappre- 
ciable. When  fluid  exists  in 
the  right  pleural  cavity^  or 
there  is  solidification  of  the 
right  lung,  the  dulness  thus 
occasioned  blends  indistin- 
guishably  with  that  of  the 
beart.  Under  favourable  con- 
ditions, however,  cardiac  dul- 
ness is  found  increased  to  the 
right  and  downward,  the  ex- 
tent of  this  increase  being  de- 
termined by  the  degree  of  the 
dilatation  of  the  right  ventri- 
cle. In  cases  of  primary  or  independent  tricuspid  insufficiency 
due  to  endocarditis,   the  right  ventricle   is  found  less  enlarged 


Fig.  to. — Relative  Dulness  in  a  Case  of 
Primary  Tricuspid  Eegurgitation. 


352 


DISEASES  OF   THE   HEART 


Fig.  71. — Uelative  Dllness  in  Case  of 
Tricuspid  Eeoukgitation,  Secondary 
TO  Dilatation  of  the  Right  Ventricle. 


(Fig.  70)  than  -when  regurgitation  takes  place  as  a  result  of  ven- 
tricular dilatation  (Fig.  71).     On  the  other  hand,  in  either  form 

(if  the  affection,  dulness  is 
greatly  increased  over  the 
right  auricle  and  the  large 
venous  trunks,  reaching  far 
beyond  the  right  sternal  bor- 
der, half-way  or  more  to  the 
right  mamillary  line.  In  most 
instances  also  there  is  increase 
of  cardiac  dulness  to  the  left, 
depending  upon  the  nature 
and  extent  of  the  accompany- 
ing disease  of  the  left  heart. 

Auscultation. — This  fur- 
nishes even  less  trustworthy 
data  than  are  obtained  by  per- 
cussion. There  is  generally 
a  blowing,  systolic  murmur, 
said  to  have  its  maximum  in- 
tensity in  the  tricuspid  area  (Fig.  72)  ;  yet  as  the  dilatation  of 
the  several  cardiac  chambers  alters  the  normal  relations  of  the 
parts,  this  murmur  may  be 
heard  most  distinctly  in  any 
one  of  several  situations.  It 
may  be  at  the  junction  of  the 
fifth  and  sixth  left  costal  car- 
tilages with  the  sternum,  over 
the  ensiform  appendix,  or 
even  to  the  right  of  the  ster- 
num in  the  third,  fourth,  or 
fifth  intercosal  spaces,  close  to 
this  bone. 

Gibson,  in  his  remarks  on 
the  Heart  in  Debility,  has 
narrated  cases  showing  that 
the  murmur  may  be  heard  in 

,1  1    1    Xi    :„j^„„^„«^    r.,,         l*'"-   72. — 1'lace    of    Maximum    Audiuilitv 

the  second   lett   mterspace  an  ,  n  .  t. 

'      _  (small  circle)  and  Area   of   Propaoa- 

inch    from    the   sternum,    in    an  tion  of  Tricuspid  Regurgitant  Murmur. 


TRICUSPID  REGURGITATION  353 

area  in  which  a  systolic  pulsation  is  also  often  observed.  In  these 
cases  there  was  also  venous  pulsation  in  the  neck,  and  hence  it 
seems  probable  that  the  murmur  was  that  of  the  disease  now  under 
discussion.  This  is  the  site  of  a  systolic  murmur  frequently  audi- 
ble in  chlorosis  and  angemia,  and  variously  explained  by  ^N^aunyn, 
Balfour,  Russell,  Bramwell,  Handford,  Foxwell,  etc.  (see  intro- 
ductory chapter),  and  therefore  caution  is  required  in  the  cor- 
rect interpretation  of  a  bruit  in  this  situation. 

The  tricuspid  murmur  has  a  blowing  quality,  is  of  no  constant 
pitch,  and  differs  much  in  loudness,  according  to  the  conditions 
that  generate  it.  It  is  often  obscured  by  other  bruits  originating 
at  other  orifices,  particularly  at  the  mitral.  If  the  auscultator  is 
experienced,  and  conditions  are  favourable^  he  may  be  able  to 
locate  different  areas  of  maximum  intensity  for  the  different  mur- 
murs, and  thus  be  able  to  determine  which  is  tricuspid,  which 
mitral,  etc. 

Regarding  the  heart-sounds  in  tricuspid  insufficiency  but  little 
need  be  said.  The  first  tone  over  the  right  ventricle  is  apt  to  be 
muffled,  even  replaced,  by  the  murmur.  The  pulmonic  second 
sound  appears  to  differ  in  different  cases.  It  would  naturally  be 
enfeebled,  in  consequence  of  the  fact  that  lessened  blood  is  expelled 
into  the  artery,  but  as  the  predisposing  mitral  or  other  disease  has 
augmented  blood-pressure  in  the  vessels  of  the  lungs,  the  second 
tone  in  the  pulmonic  area  may  be  accentuated.  However,  if  in  a 
given  case  of  gastrectasis  tricuspid  regurgitation  is  suspected,  an 
enfeeblement  of  this  second  sound  would  lend  a  measure  of  sup- 
port to  the  diagnosis. 

Lastly,  it  is  quite  common  to  hear  a  vascular  tone,  if  one  aus- 
cultates the  vein  in  which  the  positive  pulse  is  seen,  and  the  tone 
thus  obtained  is,  of  course,  synchronous  with  the  pulsation. 

Diagnosis. — Recapitulating,  I  wish  to  emphasize  the  state- 
ment that  inasmuch  as  mitral  murmurs  may  sometimes  be  heard 
with  great  intensity  over  the  right  ventricle,  and  be  conducted  far 
beyond  the  right  border  of  the  sternum,  it  is  very  unsafe  to  rely 
upon  a  murmur  in  the  tricuspid  area  in  making  a  diagnosis  of  re- 
gurgitation through  this  valve.  Certainly  it  is  so  exceptional  for 
any  considerable  leakage  to  occur  at  this  ostium  without  giving 
rise  to  the  venous  and  hepatic  pulsation  already  described,  that  in 
the  absence  of  these  pathognostic  signs  it  is  unsafe  to  declare  that 


354  DISEASES  OF  THE   HEART 

the  nuirmur  is  that  of  regurgitation.  This  has  been  impressed 
upon  nie  many  times. 

There  is  a  certain  Russian  Jew  who  exhibits  himself  to  medi- 
cal students  for  examination  because  of  his  possessing  a  musical 
murmur  of  obscure  origin.  In  his  instance  the  bruit  is  systolic, 
and  most  intense  upon  and  immediately  roundabout  the  xiphoid 
cartilage.  From  its  location,  therefore,  it  is  thought  by  many  good 
observers  to  be  a  tricuspid  regurgitant  one.  The  musical  murmur 
is,  however,  also  distinctly  audible  well  outside  the  left  nipple ;  and 
as  there  is  a  combination  of  lesions  in  this  case  it  is  very  difficult, 
if  not  impossible,  to  definitely  decide  whether  the  murmur  in 
question  is  tricuspid  or  mitral.  It  all  depends  on  the  existence 
or  not  of  a  positive  venous  pulse  in  the  jugulars.  Six  years  ago  I 
did  not  detect  such  a  pulsation ;  tw^o  years  ago  I  thought  such  a 
venous  pulse  was  present;  a  few  days  ago  (March,  1902)  there 
was  no  such  evidence  of  tricuspid  regurgitation,  and  consequently 
I  am  obliged  to  still  leave  the  question  suh  judice.  The  heart  was 
in  a  far  better  state  than  two  years  before,  and  it  is  quite  possible 
that  a  slight  relative  tricuspid  incompetence  was  accountable  for 
the  jugular  pulsation  at  that  time.  At  all  events  this  interesting 
case  is  very  exceptional,  for  ordinarily  it  is  not  a  difficult  matter 
to  determine  the  existence  of  tricuspid  leakage.  It  illustrates  that 
in  the  absence  of  a  positive  venous  pulse  in  jugulars  or  liver  one  is 
not  wise  in  declaring  a  systolic  bruit  in  the  tricuspid  area  to  be 
tricuspid. 

Prognosis.— This  may  be  said  to  depend  upon  the  nature  and 
causes  of  the  tricuspid  insufliciency.  Relative  incompetence  of 
this  valve  may  come  and  go  quickly,  but  unless  its  cause  can  be 
removed  its  tendency  is  steadily  downward,  although  death  may 
not  occur  for  weeks  or  even  months. 

Mode  and  Causes  of  Death. — The  fatal  termination  grad- 
ually results  from  either  general  or  cardiac  exhaustion,  in  conse- 
quence largely  of  malnutrition,  or  from  pressure-effects  of  the 
dropsy,  or  from  pulmonary  oedema,  or  from  some  other  terminal 
manifestation  of  the  primary  cardiac  or  lung  affection.  In  other 
words,  there  is  no  mode  of  death  peculiar  to  tricuspid  insufficiency 
per  sf.  In  8  cases  of  this  disease  Ilustedt  found  as  the  cause  of 
death  cardiac  weakness  once,  phthisis  once,  and  anaimia  once. 


CHAPTER    XI 
TRICUSPID    STENOSIS 

This  is  the  counterpart  of  mitral  stenosis,  but  is  infinitely 
more  rare.  Indeed,  it  is  said  to  be  the  rarest  of  all  valvular  de- 
fects— so  much  so  that  some  writers  speak  of  it  merely  as  a  patho- 
logical curiosity,  and  devote  very  little  space  to  its  consideration. 
It  probably  occurs  oftener  than  it  is  recognised,  and  yet  its  ex- 
treme infrequency  may  be  judged  of  by  the  fact  that,  although 
many  thousand  necropsies  are  annually  made,  only  154  cases  had 
been  recorded  in  medical  literature  up  to  the  fall  of  1896.  Of 
these,  114  collected  by  Leudet  occurred  prior  to  1888,  while  in  the 
next  eight  years  Herrick  collected  40  more.  Three  of  these  were 
his  own  cases,  and  the  total  number  was  brought  up  to  154.  It 
is  to  the  latter's  monograph  that  I  am  indebted  for  much  that,  will 
be  said  in  the  following  pages. 

Morbid  Anatomy. — -This  differs  according  to  the  group  into 
which  the  respective  case  falls,  for  tricuspid  stenosis  may  be  either 
congenital  or  acquired.  The  former  class  is  again  subdivided  into 
those  due  to  intra-uterine  endocarditis  and  those  resulting  from 
some  defect  of  development.  In  the  congenital  form  there  are 
the  usual  associated  abnormalities,  such  as  stenosis  of  the  pulmo- 
nary artery,  defective  closure  of  the  interventricular  sseptum,  and 
patency  of  the  foramen  ovale  and  ductus  arteriosus. 

When  acquired  as  a  result  of  endocarditis  tricuspid  stenosis 
presents  changes  analogous  to  those  at  the  left  auriculo-ventricu- 
lar  orifice,  thickening,  rigidity,  and  adhesion  of  the  flaps.  Vege- 
tations may  also  be  found  on  their  auricular  aspect,  and  the  neigh- 
bouring endocardium  is  apt  to  present  the  grayish-white  appear- 
ance and  thickening  characteristic  of  mural  endocarditis. 

The  shape  and  size  of  the  opening  at  the  extremity  of  the 
cusps  are  variable,  the  same  as  in  mitral  stenosis.  The  conditions 
are  also  such  as  occasion  incompetence  as  well  as  obstruction.    The 

355 


356  DISEASES   OF   THE   HEART 

tendinous  cords  and  papillary  ninscles  may  in  some  cases  also 
show  the  changes  of  endocarditis.  In  the  great  majority  of  cases 
tricuspid  stenosis  is  associated  with  other  valvular  diseases,  as 
shown  in  the  annexed  tables  taken  from  Lendet  and  Herrick : 

Lt'udet 

Tricuspid  stenosis  alone 11 

Tricuspid  stenosis  with  mitral  stenosis 78 

Tricuspid  stenosis,  mitral,  and  aortic  stennsis 21 

Tricuspid  stenosis  and  pulmonary  stenosis 3 

Tricuspid  stenosis,  mitral  stenosis,  and  pulmonary  stenosis. . .  1 

Herrick 

Tricuspid  stenosis 1 

Tricuspid  and  mitral  stenosis 18 

Tricuspid  and  pulmonary  stenosis 0 

Tricuspid,  mitral,  and  aortic  stenosis 18 

Tricuspid,  mitral,  and  pulmonary  stenosis 1 

Tricuspid,  mitral,  aortic,  and  pulmonary  stenosis . .  1 

Tricuspid  stenosis  and  endocardium  of  the  left  auricle 1 

Tricuspid  stenosis  and  aortic  stenosis 0 

The  changes  observed  in  the  walls  and  cavities  of  the  heart 
are  in  part  secondary  to  the  tricuspid  stenosis,  and  in  part  to  the 
coexisting  lesions  of  other  orifices  and  valves.  The  right  ventri- 
cle usually  exhibits  combined  hypertrophy  and  dilatation,  in  con- 
sequence largely  of  the  conjoined  mitral  defect,  but  if  the  tricus- 
pid obstruction  is  great,  with  but  little  if  any  regurgitation,  the 
ventricle  is  diminished  rather  than  enlarged  in  size.  The  cham- 
ber upon  which  the  stenosis  chiefly  reacts  is  the  right  auricle,  and 
hence  this  is  more  or  less  hypertrophied  and  dilated,  according  to 
the  degree  of  the  stenosis.  It  has  been  known  to  reach  a  size  of 
two  or  three  times  the  normal,  but  because  of  the  thinness  of  its 
wall  the  right  auricle  rarely  undergoes  much  compensatory  hyper- 
trophy. The  degeneration  of  the  myocardium  is  such  as  is  often 
found  in  other  valvular  diseases,  and  in  one  of  Herrick's  cases  the 
right  ventricle  was  covered  by  a  thick  layer  of  subpericardial  fat. 

Etiology. — Cases  of  this  disease  originating  after  birth  are 
due  to  endocarditis,  and  as  in  other  forms  of  valvular  defect  of  this 
origin,  articular  rlicumiitisin  aj)])ears  to  be  its  chief  exciting  cause. 
Herrick  states  that  of  the  154  collected  cases,  30  per  cent  gave  a 
history  of  antecedent  rheumatism.  He  also  says  that  syphilis  has 
been  assigned  as  a  cause,  and  that  Leudet  regards  the  puerperium 
as  also  an  etiological  factor.     This  hitter  fact  may  possibly  have 


TRICUSPID  STENOSIS  357 

a  bearing  on  the  far  greater  frequency  of  tricuspid  stenosis  in  the 
female  than  in  the  male  sex.  The  disproportion  of  the  two  sexes  in 
this  disease  is  far  too  patent  to  be  merely  accidental,  Gibson  stat- 
ing that  of  146  cases  of  tricuspid  obstruction,  114  occurred  in 
females  and  32  in  males. 

This  disease  also  occurs  most  frequently  in  the  early  decades  of 
life,  the  majority  of  cases  falling  between  the  twentieth  and  thir- 
tieth years.  In  this  respect  it  is  not  peculiar,  for,  as  we  know, 
valvular  diseases  of  rheumatic  origin  are  much  more  frequent  in 
the  young  than  in  j^ersons  of  middle  or  advanced  age. 

Symptoms. — The  fact  that  the  ablest  and  most  experienced 
clinical  observers  have  failed  to  recognise  the  existence  of  tricus- 
pid stenosis  during  life,  and  that  in  most  cases  it  has  first  been 
detected  on  the  autopsy  table,  may  be  regarded  as  proof  that  there 
is  no  symptomatology  peculiar  to  this  affection.  Its  clinical  mani- 
festations, even  when  such  exist,  are,  moreover,  apt  to  be  obscured 
by  those  belonging  to  the  associated  lesions.  Thus,  although  ob- 
struction at  the  tricuspid  orifice  leads  to  stasis  in  the  systemic 
veins,  the  liver,  and  other  abdominal  organs,  mitral  disease  does 
the  same ;  and  as  the  physical  signs  of  this  latter  affection  gener- 
ally mask  those  of  the  tricuspid  defect,  the  symptoms  are  quite 
likely  to  be  attributed  to  the  disease  in  the  left  heart. 

Tricuspid  stenosis  tends  to  limit  the  amount  of  blood  sent  to 
the  lungs  and  left  auricle,  and  therefore  there  is  nothing  in  this 
disease  tending  to  produce  dyspnoea  of  effort  and  other  symptoms 
referable  to  pulmonary  congestion.  In  fact,  were  the  tricuspid 
lesion  to  exist  alone,  the  effect  on  the  lungs  would,  like  that  of  pul- 
monary stenosis,  be  one  of  ansemia  with  its  tendency  to  tubercu- 
losis ;  and  it  is  here  worthy  of  note  that  in  the  single  instance  in 
which  Hustedt  ascertained  the  cause  of  death,  this  was  "  phthisis." 
It  is  plain,  therefore,  that  when  we  leave  out  of  consideration  the 
pulmonary  symptoms  due  to  conjoined  mitral  disease,  we  must 
seek  the  clinical  features  of  tricuspid  stenosis  in  all  those  perver- 
sions of  function  incident  to  visceral  hypersemia  and  in  the  effects 
and  manifestations  of  general  venous  engorgement. 

The  jugulars  are  distended,  and  when  hypertrophy  of  the  right 
auricle  is  marked,  these  veins  are  likely  to  exihibit  a  negative — 
that  is,  diastolic-presystolic  pulsation.  This  was  the  case  in  one 
of  my  patients  in  whom  physical  signs  led  me  to  suspect  the  exist- 


358  DISEASES  OF   THE   HEART 

ence  of  tricuspid  narrowing,  bnt  in  which  case,  unfortunately,  a 
post-mortem  examination  could  not  be  obtained.  The  liver  bears 
the  main  brunt  of  the  secondary  stasis,  and  is  consequently  greatly 
eidarged,  perhaps  tender,  and  there  is  furthermore  a  growing  tend- 
ency to  ascites  and  cedenui. 

I  have  had  the  good  fortune  to  observe  a  patient  in  whom  dur- 
ing life  there  were  the  classical  signs  of  both  mitral  and  tricuspid 
stenosis,  as  will  be  subsequently  described,  and  whose  heart  pre- 
sented such  interesting  post-mortem  findings  that  the  case  will  be 
here  introduced. 

The  patient  was  a  Polish  Jew  under  the  care  of  Dr.  Kaczorow- 
ski,  by  whom  he  was  brought  to  me.  His  age  was  given  as  forty- 
three,  and  for  six  years  he  had  been  unable  to  work  on  account  of 
shortness  of  breath.  There  was  a  history  of  scarlatina  in  child- 
hood and  of  articular  rheumatism  fifteen  3'ears  before  I  saw  him, 
but  further  particulars  were  too  vague  to  be  trustworthy. 

His  sym})toms  were  dyspncra  on  exertion  and  a  cough,  which 
had  existed  for  six  weeks.  The  liver  was  engorged  and  palpable 
for  a  distance  of  3  inches  below  the  costal  arch,  anJ  there  was 
distention  of  the  external  jugulars. 

The  heart  was  greatly  enlarged  in  all  diameters,  and  there 
were  two  separate  and  distinct  presystolic  murmurs,  one  at  the 
apex  and  the  other  close  to  the  xiphoid  cartilage.  The  diagnosis 
of  a  double  stenosis  was  made,  tricuspid  as  well  as  mitral,  a;nd  the 
patient  Avas  not  lost  sight  of,  although  only  seen  twice  in  the  sub- 
sequent sixteen  months,  the  last  occasion  being  five  weeks  prior  to 
death.  Some  four  months  before  the  fatal  issue  he  began  to  have 
O'dema  of  the  lower  extremities,  and  to  suffer  much  from  difficulty 
of  l)reathing,  amounting  to  orthopncea.  The  anasarca  increased 
raj)idly  and  soon  invaded  the  scrotum,  Avhich  became  so  distended 
that  he  was  compelled  to  let  it  hang  through  a  large  opening  cut 
for  the  purpose  in  the  seat  of  his  chair.  Cathartics  afforded  but 
slight  and  transient  relief,  and  upon  receiving  an  urgent  request 
from  the  attending  physician  to  suggest  some  means  of  lessening 
the  painful  scrotal  distention  I  advised  tapping,  although  it  was 
realized  that  this  would  ameliorate  the  condition  for  only  a  short 
time. 

When  at  length  T  found  time  to  visit  tlio  jxmr  fellnw  his  ])light 
was  truly   ]»iliiil»l('.      lie  was   in   a  chair,   which   he  had   scarcely 


TRICUSPID  STENOSIS  359 

qiutted  for  many  weeks,  and  he  presented  signs  of  moderate  as- 
cites as  well  as  extensive  wdema  of  the.lower  extremities.  The 
scrotum  was  as  large  as  a  child's  head,  of  a  purplish-red  colour, 
very  hard  to  pressure,  and  bathed  in  bloody  serum,  which  trickled 
drop  by  drop  into  a  basin  underneath  his  chair.  Owing  to  the 
inability  of  the  patient  to  move  or  sit  in  any  other  position  ex- 
amination was  difficult.  But  so  far  as  it  was  possible  to  deter- 
mine, the  cardiac  findings  were  essentially  as  found  and  recorded 
fifteen  months  earlier. 

The  pulse  was  weak,  moderately  accelerated,  and  irregular. 
As  cathartics,  diuretics,  and  digitalis  had  all  been  used  freely,  and 
proved  of  very  little  efficacy,  no  additional  suggestions  could  be 
offered,  and  the  poor  svifferer  was  reluctantly  left  to  wear  out  his 
few  remaining  weeks  of  life  as  best  he  might.  The  blessed  release 
came  about  five  weeks  later,  and  Dr.  W.  A.  Evans  made  the 
autopsy. 

There  was  much  subcutaneous  oedema  and  gangrene  of  the 
penis,  scrotum,  and  one  of  the  large  toes.  The  peritonaeum  and 
right  pleural  cavity  contained  clear  serum.  The  various  organs 
showed  the  usual  changes  of  long-standing  congestion.  The  heart 
was  enormously  enlarged  on  both  sides  and  was  hardened  by  Kais- 
erling's  solution  without  being  opened  (Plate  III).  However,  an. 
attempt  was  made  to  discover  the  condition  of  the  tricuspid  orifice 
by  passing  the  fingers  through  the  great  venous  opening  in  the 
right  auricle.  The  tricuspid  ostium  admitted  three  fingers  to  the 
second  joint  instead  of  four,  as  is  normally  the  case,  and  it  felt 
firm  and  resisting.  Moreover,  the  valve  could  be  felt  projecting 
across  the  opening. 

When  at  length  the  specimen  had  become  hardened  and  it  was 
opened  an  interesting  combination  of  lesions  was  presented.  The 
mitral  orifice  was  a  mere  buttonhole  slit,  and  the  endocardium  of 
the  left  auricle  showed  the  whitish,  thickened  appearance  denot- 
ing prolonged  high  blood-pressure,  and  its  wall  was  hypertroj)hied. 
The  valve  projected  like  a  cone  into  the  cavity  of  the  ventricle, 
which  was  both  hypertrophied  and  dilated.  The  cords  were  fused 
and  presented  unmistakable  evidence  of  old  endocarditis.  There 
was  some  thickening  of  the  aortic  cusps,  which  had  caused  moder- 
ate obstruction  at  that  orifice,  a  conclusion  justified  by  the  en- 
largement instead  of  atrophy  of  the  left  ventricle  usually  found 


360  DISEASES   OF   THE   HEART 

in  mitral  stenosis.  Yet  during  life  this  aortic  lesion  had  not  pro- 
duced recognisable  signs  aside  from  enfeeblement  of  the  aortic  sec- 
ond soimd,  which  had  been  attributed  to  the  smallness  of  the  blood- 
stream ejected  into  the  aorta  bv  reason  of  the  mitral  disease. 

The  pulmonary  artery  i)resented  a  remarkably  extensive 
atheroma,  due  evidently  to  the  long-standing  and  extreme  pressure 
to  which  this  vessel  had  been  subjected.  The  pulmonary  orifice 
was  relatively  dilated,  and  the  valves  were  of  increased  size.  Con- 
sequently, the  conclusion  seemed  warranted  that  relative  insuffi- 
ciency of  this  valve  had  existed  and  had  contributed  to  the  enor- 
mous dilatation  of  the  right  ventricle.  This  very  great  hyper- 
trophy and  dilatation  had  been  recognised  during  life,  but  had 
been  put  down  as  secondary  to  the  extreme  mitral  obstruction. 
The  pulmonary  regurgitation  either  failed  to  produce  a  diastolic 
murmur,  or  it  had  been  overlooked.  The  pulmonic  second  tone 
was  noted  as  feeble,  but  this  was  thought  due  to  the  diminished 
amount  of  blood  sent  through  the  tricuspid  ring.  I  feel  quite  cer- 
tain that  an  audible  diastolic  murmur  did  not  exist. 

The  right  auricle  was  not  only  strikingly  dilated,  but  its  wall 
was  thickened,  and  its  lining  membrane  also  showed  by  its  appear- 
ance to  what  a  high  degree  of  pressure  this  chamber  had  been  sub- 
jected. 

The  tricuspid  ring  was  rigid,  barely  admitting  the  tips  of  four 
fingers.  The  valve  leaflets  were  very  considerably  thickened  and 
partially  united,  so  that  the  opening  was  considerably  smaller  than 
the  actual  tricuspid  ring.  It  was  the  thick  and  rigid  edge  of  the 
posterior  flap  that  was  felt  in  the  preliminary  examination. 

This  interesting  specimen  was  submitted  to  Dr.  Gustav  Fiit- 
terer,  and  at  first  he  was  inclined  to  doubt  the  existence  of  an 
appreciable  tricuspid  stenosis.  Yet,  after  a  careful  examination 
of  the  right  heart,  he  arrived  at  the  opinion  that  in  consideration 
of  the  marked  dilatation  of  both  the  right  ventricle  and  auricle 
and  the  disproportionate  smallness  of  the  tricuspid  ring,  together 
with  its  firmness  and  thickening,  and  the  condition  of  its  flaps, 
one  could  not  escape  the  conclusion  that  actual  stenosis  of  the  ring 
had  existed. 

Moreover,  the  endocardium  of  the  ventricle  displayed  slight 
evidence  of  previous  inflammation,  probably  the  same  process  that 
had  thickened  the  edges  of  the  tricuspid  valve.     Nevertheless,  it 


TRICUSPID  STENOSIS 


361 


was  Dr.  Flitterer's  opinion  that  the  symptoms  had  been  caused 
more  by  the  mitral  narrowing  and  the  relative  pulmonary  regurgi- 
tation than  by  the  stenosis  of  the  tricuspid  ostium.  However  this 
may  be,  I  can  only  assert  that  it  had  been  sufficient  to  occasion 
very  positive  clinical  signs,  else  I  should  not  have  suspected  and 
diagnosticated  so  rare  a  lesion  in  the  presence  of  a  pronounced 
mitral  disease  to  which  one  might  very  naturally  have  attributed 
the  symptoms  of  stasis.  I  must  therefore  stand  by  my  belief  that 
to  the  tricuspid  stenosis  is  to  be  attributed  a  not  unimportant  share 
in  the  production  of  the  unusual  degree  of  general  venous  stasis 
as  compared  with  the  pulmonic.  The  right-sided  hydrothorax,  dis- 
covered post  mortem,  furnished  proof  of  the  enormous  stasis  that 
had  been  present  in  the  cavity  of  the  right  auricle. 

At  all  events  this  case  illustrates  the  influence  of  right  heart 
lesions  in  the  causation  of  general  venous  and  visceral  stasis,  while 
the  gangrene  bore  witness  to  the  profound  emptiness  of  the  aortic 
system. 

Physical  Signs. — Inspection. — A  perusal  of  Herrick's  col- 
lected cases  convinces  one  that  there  is  nothing  in  the  appearance 
of  these  patients  to  distinguish  them  from  those  with  mitral  dis- 
ease in  the  last  stages  of 
broken  compensation.  In 
Case  27  of  his  series  venous 
pulse  was  noticed,  but  ordi- 
narily there  is  nothing  more 
than  the  ocular  evidence  of 
venous  and  capillary  stasis. 

Palpation. — The  pulse  is 
small  and  weak,  and  may  be 
regular  or  irregular,  and  mod- 
erately or  greatly  accelerated. 
In  Broadbent's  case  (N^o.  25 
of  Herrick's  series)  the  pulse 
was  reported  as  100,  small, 
and  irregular,  while  in  Eustis 
Smith's  case  (No.  29)  it  was 
recorded  as  only  60  and  small. 

There  is  nothing  in  such  statements  that  might  not  also  apply 

to  the  pulse  in  mitral  disease.     Palpation  of  the  prsecordia  is  usu- 
25 


Fig.  T3. — Location  of  Thrill  and  Murmuk 
IN  A  Typical  Case  of  Tricuspid  Stenosis. 


362 


DISEASES   OF   THE   HEART 


ally  negative  so  far  as  the  tricuspid  lesion  is  concerned,  but  in 
some  instances  there  may  be  a  short,  thumping  impulse  in  the  epi- 
gastrium similar  to  but  distinct  from  that  of  the  associated  mitral 
stenosis.  This  was  pronuunecd  in  the  case  I  have  narrated.  There 
was  also  a  short  presystolic  thrill  in  the  sulcus  between  the  ensi- 
form  appendix  and  the  left  costal  cartilages  (Fig.  73),  which  Avas 
plainly  shorter  and  less  distinct  than  that  felt  at  the  apex.  Be- 
tween these  two  tliere  was  a  space  in  which  no  presystolic  thrill 
could  be  detected,  and  it  was  this  fact  that  first  riveted  my  atten- 
tion. This  short  thrill  ran  u])  to  and  ended  abruptly  with  the 
thumping  systolic  shock  mentioned. 

It  is  conceivable  that,  owing  to  the  heart  lying  nearer  to  the 
median  line  than  usual,  a  presystolic  thrill  and  sharp  systolic 
shock  of  mitral  stenosis  might  be  felt  in  the  tricuspid  area.  Con- 
sequently, the  recognition  of  these  signs  in  this  area  alone  would 
not  be  so  suspicious  as  was  the  detection,  in  my  case,  of  these  pal- 
patory phenomena  in  two  separate  and  distinct  situations. 

Percussion. — Cardiac  dulness  is  increased  over  the  right  auri- 
cle— that  is,  at  the  right  of  the  sternum — but  this  is  not  distinctive, 

since  it  occurs  likewise  in  mi- 
tral disease  (Fig.  74).  In 
tricuspid  stenosis  it  is  likely 
to  be  particularly  well  marked. 
It  may  be  said,  therefore,  that 
the  evidence  derived  by  per- 
cussion is  valuable,  but  not 
positive. 

Auscultation.  —  Unfortu- 
nately the  results  of  this  means 
of  examination  are  also  likely 
to  be  very  indefinite.  Even  if 
a  murmur  generated  at  the 
tricuspid  orifice  exists,  it  is 
likely  to  be  confused  with  or 
indistinguishable  from  mur- 
murs produced  elsewhere,  par- 
ticularly mitral  l)ruits.  In  my  case,  as  in  Broadbent's  (No.  15  of 
Herrick's  series),  there  was  a  distinctive  murmur  in  the  tricuspid 
area.     In  my  patient  a  presystolic  murmur  existed  in  the  very 


Fio.  74. — Relative  Cakdi a        ■ 
Typi<:ai-  Case  of  Thhi  si-id  Stex 


TRICUSPID  STENOSIS  363 

situation  in  which  the  thrill  was  detected,  and  it  was  much  shorter 
than  that  at  the  mitral  area,  was  of  a  Somewhat  different  pitch, 
and  terminated  in  a  sharp  thud,  the  same  as  in  Broadbent's  case. 
But  this  was  not  all ;  when  the  stethoscope  was  passed,  little  by  lit- 
tle, from  the  long,  rolling  mitral  bruit  towards  the  ensiform,  it  was 
noted  that  there  was  a  space  in  which  the  mitral  murmur  became 
lost,  while  a  trifle  nearer  the  sternum  another  area  was  reached 
in  which  another  and  shorter  presystolic  murmur  became  audible. 
This  fact  showed  plainly  that  there  were  two  areas  of  maximum 
intensity  for  these  two  presystolic  murmurs,  which  fact  convinced 
me  that  I  had  to  do  with  two  entirely  separate  and  distinct  bruits. 

It  may  be  objected  that  this  murmur  in  the  epigastrium  was 
the  pulmonary  regurgitant  murmur  transmitted  to  that  point. 
But  in  reply  to  this  possible  objection  I  need  only  point  out  that 
although  both  murmurs  are  diastolic,  that  of  pulmonary  regurgita- 
tion falls  in  the  early  part  of  diastole  immediately  after  the  sec- 
ond sound,  while  a  presystolic  one  occurs  just  before  the  first 
sound  at  the  end  of  diastole. 

Theoretically  and  practically,  therefore,  in  endeavouring  to 
establish  the  existence  of  tricuspid  stenosis,  one  must  search  for 
auscultatory  signs  in  the  tricuspid  area,  yet  must  remember  that 
owing  to  the  enlargement  of  the  right  heart  the  position  of  the 
tricuspid  orifice  becomes  changed,  so  that  the  tricuspid  area  is  a 
wide  one.  Broadbent  detected  the  murmur  in  the  fifth  right  in- 
terspace, close  to  the  sternum. 

Finally,  in  most  cases  of  this  lesion  more  or  less  regurgitation 
is  permitted,  and  hence  the  tricuspid  disease  may  declare  itself 
by  a  systolic  murmur,  the  presystolic  being  either  absent  or  so 
short  as  to  entirely  escape  recognition  in  the  presence  of  the  regur- 
gitant bruit.  In  but  12  of  the  154  cases  was  the  tricuspid  orifice 
alone  the  seat  of  disease,  which  shows  its  rarity  apart  from  asso- 
ciated defects.  I  should  fancy  that  when  it  exists  alone,  it  ought 
to  be  recognised  more  easily  than  when  combined,  and  hence  ob- 
scured by  coexisting  disease. 

Diagnosis.  ^ — Owing  partly  to  the  indefiniteness  of  the  physi- 
cal signs  and  partly  to  their  being  obscured  by  those  of  associated 
valvular  lesions,  the  diagnosis  of  tricuspid  stenosis  is  generally 
first  made  on  the  autopsy  table.  Some  of  the  ablest  clinical  ob- 
servers  believe   that    an   intra-vitam   diagnosis   must    always   be 


364  DISEASES   OF   THE   HEART 

problematic,  and  that  when  made  correctly  it  is  a  matter  of  for- 
tuitous circumstance.  One  should  not  feel  chagrined,  therefore, 
over  his  failure  to  recognise  the  existence  of  this  disease  during 
life.  Conversely,  should  he  be  so  fortunate  as  to  have  his  ante- 
mortem  diagnosis  corroborated  by  the  necropsy,  he  should  not  take 
pride  to  himself,  but  rather  congratulate  himself  upon  the  fact 
that  in  that  particular  case  the  lesion  had  furnished  recognisable 
physical  signs. 

Prognosis. — Xotwithstanding  the  fact  that  one  of  Leudet's 
patients  is  reported  to  have  reached  the  age  of  sixty-four,  the  pros- 
pect of  long  life  is  not  good  in  cases  of  this  disease.  Death  over- 
took the  majority  of  his  cases  between  the  ages  of  twenty  and 
thirty.  This  brevity  of  life  is  due  probably  not  so  much  to  the 
tricuspid  obstruction  itself  as  to  its  association  with  other  valve- 
lesions  so  pronounced  as  to  make  it  a  matter  of  wonder  that  pa- 
tients live  as  long  as  they  do.  When  compensation  begins  to  fail 
there  is  small  prospect  of  its  restoration.  The  immediate  prog- 
nosis depends  upon  the  severity  of  symptoms  as  well  as  upon  the 
number  and  degree  of  associated  lesions.  Albuminuria,  ascites, 
hydrothorax,  etc.,  indicate  the  terminal  stage  of  the  disease,  and 
yet  proper  care  and  management  may  extend  the  life  of  a  patient 
many  months  after  the  urgency  of  symptoms  has  compelled  him 
to  seek  medical  aid.  Most  of  the  cases  reported  by  Ilerrick  Avere 
under  observation  from  a  few  months  to  a  year  or  longer. 

Mode  and  Causes  of  Death. — Death  occurred  suddenly  in 
one  of  Ilerrick's  cases,  but  nothing  was  found  at  the  post-mortem 
examination  to  explain  it,  further  than  the  ordinary  changes  in 
hearts  with  other  valvular  diseases.  As  a  rule  death  comes  slowly 
from  gradual  cardiac  exhaustion,  or  probably  as  a  result  of  an 
approaching  standstill  in  the  circulation,  due  to  reversal  of  the 
normal  blood-pressure  within  the  arterial  and  venous  systems.  In 
Ilustcdt's  single  case  already  mentioned  the  cause  of  death  was 
put  down  as  "  phthisis,"  which  emphasizes  the  fact  that  death 
is  likely  to  be  the  indirect  rather  than  the  direct  result  of  this 
valvular  defect. 


CHAPTER    XII 
PULMONARY    REGURGITATION 

This  form  of  valvular  disease  is  the  corollary  of  aortic  insuffi- 
ciency, but  is  infinitely  more  uncommon,  and  unassociated  v^ith 
other  valvular  lesions  is  very  rare.  Although  I  have  observed  a 
single  instance  of  chronic  organic  pulmonary  incompetence,  as 
determined  by  the  history  and  clinical  signs,  I  am  indebted  for 
the  most  of  what  will  be  said  to  Barie's  paper  on  the  subject. 

Morbid  Anatomy. — This  depends  largely  upon  the  cause  of 
the  disease.  Thus  we  recognise  two  chief  groups:  (1)  A  func- 
tional or  relative  incompetence  in  which  the  pulmonary  artery 
and  ring  are  so  dilated  that  the  valves  cannot  close  the  orifice, 
but  are  themselves  not  responsible  for  the  regurgitation.  ( 2 )  The 
form  in  which  the  leak  results  from  structural  changes  in  the 
valve-segments.  Thus  far  this  disease  is  the  counterpart,  both 
pathologically  and  etiologically,  of  the  other  valvular  lesions  that 
have  been  considered,  but  the  second  group  of  pulmonary  regurgi- 
tant lesions  is  again  divisible  into  the  congenital  and  the  acquired. 
In  this  respect  it  conforms  with  what  we  know  of  right-heart  de- 
fects and  diifers  from  valvular  diseases  of  the  left  heart,  since 
congenital  affections  of  the  mitral  and  aortic  valves  are  exceed- 
ingly rare. 

In  relative  insufficiency  of  the  pulmonary  valve  the  artery  and 
ostium  are  found  stretched,  and  the  former  may  show  the  changes 
of  atheroma,  while  the  leaflets  are  elongated  and  broadened  in 
consequence  of  the  strain  to  which  they  have  been  subjected,  yet 
in  other  particulars  are  quite  likely  to  be  free  from  disease.  This 
was  the  case  in  the  patient  with  mitral  and  tricuspid  stenosis 
whose  history  was  narrated  in  the  preceding  chapter. 

In  those  instances  in  which  the  regurgitation  is  the  result  of 
endocarditis,  the  changes  are  the  same  as  in  other  valvular  defects 
of  the  same  origin,  and  hence  do  not  need  to  be  repeated  in  ex- 

365 


366  DISEASES  OF  THE  HEART 

tenso.  I  may  only  add  that  the  valve-segnients  have  in  several 
cases  been  found  torn  into  shreds  in  consequence  of  inflammatory 
softening.  Xot  infrequently,  according  to  Barie,  the  changes  are 
such  as  to  have  led  to  more  or  less  obstruction,  as  shown  in  23  out 
of  43  cases  of  pulmonary  regurgitation. 

Congenital  regurgitation  at  this  orifice  is  certainly  rare,  and 
yet  Barie  is  also  authority  for  the  statement  that  it  was  discovered 
in  10  out  of  34  cases.  In  this  form  regurgitation  is  permitted  in 
consequence  of  defects  in  the  formation  of  the  valve.  In  a  three 
and  a  half  months'  infant,  cited  by  Barie,  there  was  a  rudimentary 
cusp  which  allowed  a  stream  of  water  poured  into  the  artery  to 
leak  through  into  the  right  ventricle.  In  Bouillaud's  case  the 
orifice  was  covered  by  a  membranous  partition  having  a  circular 
opening  at  its  centre  6  millimetres  in  diameter.  A  mere  hint  of 
an  attempt  at  the  subdivision  of  this  membrane  into  segments  was 
shown  by  the  presence  of  three  folds  upon  its  convex  aspect. 

The  secondary  effects  upon  the  heart  are  important.  In  the 
congenital  cases  there  is  usually  discovered  a  defective  closure  of 
the  interventricular  sai-ptum  or  patency  of  the  ductus  arteriosus, 
the  same  as  in  congenital  pulmonary  obstruction.  In  acquired 
cases,  whether  relative  or  structural,  the  right  ventricle  is  found 
dilated,  or  both  hypertrophied  and  dilated,  the  same  as  with  the 
left  ventricle  in  cases  of  aortic  regurgitation.  Moreover,  in  con- 
sequence of  the  easy  stretching  of  the  right  auriculo-ventricular 
ring,  this  orifice  is  dilated,  and  the  tricuspid  valve  is  also  incom- 
petent. 

In  cases  in  which  pulmonary  insufficiency  has  been  the  only 
valvular  defect  the  right  heart  alone  is  enlarged,  the  left  chambers 
being  small  and  looking  like  mere  appendages  in  comparison  with 
the  right.  This  appearance  is  not  usual,  however,  because  of  the 
coexistence  of  other  valvular  disease  at  the  mitral  or  aortic  ostia 
that  have  led  to  secondary  enlargement  of  the  left  half  of  the 
heart.  Finally,  the  myocardium  evinces  the  degenerative  effects 
of  long-standing  strain  and  stasis,  Mliich  have  been  already  de- 
scribed in  ])roec'ding  pages. 

Etiology. — In  the  form  of  pulniouai-y  regurgitation  most  fre- 
quently recognised — namely,  the  secondary  or  relative — the  imme- 
diate causative  element  is  abnormally  high  and  prolonged  blood- 
jiressure  in  the  pulmonary  artery.     This  in  turn  is  due  to  disease 


PULMONAEfY   REGURGITATION  367 

« 

of  the  left  heart  or  of  the  kings.  It  is  in  extreme  and  long-stand- 
ing mitral  stenosis,  therefore,  that  secondary  incompetence  of  the 
pulmonary  valve  is  oftenest  encountered. 

Obstruction  or  regurgitation  at  the  aortic  orifice  may  also  pro- 
duce pulmonary  incompetence  after  having  set  up  stretching  of 
the  left  auriculo-ventricular  ring  and  relative  mitral  regurgitation. 
Great  increase  of  blood-pressure  in  the  pulmonic  system  is  so  com- 
mon and  necessary  a  result  of  most  cardiac  and  many  pulmonary 
diseases  that  it  is  probable  that  the  regurgitation  now  considered 
takes  place  far  more  frequently  than  it  is  recognised  clinically. 

Of  those  cases  in  which  the  valve  itself  is  diseased  the  most 
frequent  cause  is  acute  endocarditis.  This  may  be  of  rheumatic 
origin,  but  it  is  more  often  septic,  and  therefore  a  localization  of 
pus  or  pneumococcus  infection.  It  occurs  in  the  puerperium, 
therefore,  the  same  as  malignant  endocarditis  in  other  situa- 
tions. 

The  causes  of  the  congenital  form  of  pulmonary  regurgita- 
tion are  intra-uterine  endocarditis  and  developmental  defects, 
whether  due  to  inflammation  or  not. 

Symptoms. — In  those  cases  in  which  pulmonary  regurgita- 
tion is  secondary  to  pre-existing  mitral  or  aortic  disease,  the  symp- 
toms of  these  latter  afi^ections  generally  obscure  those  referable 
to  the  former,  if  indeed  any  new  ones  are  developed.  The  patients 
already  suffer  from  the  effects  of  pronounced  stasis  in  the  lungs 
and  venous  system,  and  when  the  pulmonary  valves  yield  to  the 
strain  and  leak,  the  force  of  the  regurgitant  stream  is  thrown  upon 
the  already  overburdened  and  dilated  right  ventricle.  The  pro- 
pelling power  of  this  portion  of  the  heart  is  thereby  lessened,  and 
the  congestion  everywhere  present  is  augmented — but  as  this  con- 
dition has  come  on  gradually,  it  is  put  down  as  only  a  further 
manifestation  of  the  inevitable  asystolism. 

With  greater  dilatation  of  the  right  ventricle  the  tricuspid  ring 
stretches  and  tricuspid  regurgitation  is  added.  This  leak  is  more 
easily  recognised  than  is  the  pulmonic,  and  accordingly  the  still 
more  urgent  stasis  that  now  comes  on  is  attributed  to  the  tricuspid 
incompetence,  and  the  pulmonary  insufficiency  is  overlooked.  The 
seriousness  of  relative  pulmonary  incompetence  consists,  there- 
fore, not  so  much  in  the  addition  of  any  new  and  characteristic 
subjective  symptoms  as  in  the  fact  that  it  intensifies  those  already 


36S 


DISEASES   OF   THE   HEART 


existing,  while  rendering  the  prospect  of  the  j^atient's  betterment 
practically  nil. 

Objective  symptoms — that  is,  clinical  signs  of  this  complica- 
tion— are  present,  theoretically  at  least,  and  when  recognisable 
consist  in  a  weakening  or  impurity  of  the  pulmonic  second  sound, 
or  in  a  soft  diastolic  murmur,  heard  in  the  second  and  third  left 
intercostal  spaces. 

The  form  M'hich  chiefly  interests  us  at  this  time  is  the  primary 
or  organic,  which,  either  as  a  congenital  or  acquired  lesion,  exists 
independently  of  any  other  valvular  or  lung  disease.  Does  this 
produce  distinctive  subjective  symptoms  ?  To  this  query  I  think 
one  must  reply  that  not  only  does  it  not  display  distinctive  symp- 
tomatology, but  it  sometimes  pursues  a  latent  course  for  many 
years.  In  most  of  the  cases  cited  by  Barie  the  patients  displayed 
dyspna3a  and  other  ordinary  tokens  of  cardiac  disease,  as  cyanosis 
and  venous  congestion,  that  every  now  and  then  went  on  to  the 
production  of  anasarca,  albuminuria,  etc.,  but  which  were  not  in 
any  way  peculiar. 

That  the  disease  may  be  latent  for  many  years  is  proved  not 

only  by  Bouillaud's  patient 
who,  in  spite  of  her  congenital 
pulmonary  defect,  attained 
the  age  of  twenty-four,  but 
also  by  a  case  that  came  to  my 
notice  nearly  ten  years  ago. 
Most  unfortunately  an  au- 
topsy could  not  be  secured, 
and  hence  a  post-mortem  con- 
firmation of  my  diagnosis  was 
not  had.  Yet  if  })hysical 
signs  (*()unt  for  anything,  then 
this  case,  as  will  be  seen  by 
tlie  recital,  was  one  of  pulmo- 
nary regurgitation  unassoci- 
ated  with  other  valve  defects. 
The  ])atient  was  a  married 
woman  of  fifty-eight  years  of 
age  who  had  given  birth  to  eight  children  without,  she  said,  any 
greater  difficulty  than   is  experienced  l)y   most  healthy   women. 


Fig.  75. — Area  of  Deep-seated  Cakdiac 
DiLNEss  IN  Case  ok  Pulmonary  Reolk- 
GITATION  (p.  368). 


PULMONAltY  REGURGITATION 


369 


She  was  short  and  slight,  and  although  she  stated  she  had  known 
of  her  heart-disease  since  her  eighth  year^  it  had  never  occasioned 
her  any  particular  discomfort.  At  the  time  of  her  consulting  me 
she  had  been  weak,  nervous,  and  annoyed  by  palpitations  for  sev- 
eral weeks,  but  had  objected  to  seeking  medical  aid  because  of 
prejudice  and  the  discovery,  years  before,  that  the  ordinary  heart 
medicines  did  not  agree  with  her. 

She  showed  moderate  cyanosis  and  distention  of  the  external 
jugular  veins,  but  no  oedema,  and  she  did  not  complain  of  short- 
ness of  breath.  The  radial  pulses  were  equal,  moderately  accel- 
erated, irregular  in  force,  and 
occasionally  intermittent.  But 
their  particularly  noticeable 
feature  was  their  smallness 
and  feebleness.  There  was  evi- 
dent, but  not  great,  enlarge- 
ment of  the  liver.  Thus  far 
there  was  nothing  in  the  ex- 
amination of  the  patient  to 
impress  me  as  unusual. 

When,  however,  explora- 
tion of  the  heart  was  begun,  I 
was  at  once  struck  by  the  for- 
cible and  extensive  cardiac 
impulse,  which  reached  from 
the  left  nipple  into  the  epigas- 
trium, quite  across  the  median 
line  to  the  right  costal  carti- 
lages, and  as  far  downward  as 
to  the  level  of  the  eighth.  This  was  not  at  once  recognised  as  the 
impulse  of  the  enormously  hypertrophied  right  ventricle,  but  by 
carefully  studying  the  apex-beat,  and  by  determining  the  area  of 
deep-seated  cardiac  dulness  (Fig.  75),  I  became  convinced  that  it 
was  the  right  and  not  the  left  ventricle  which  was  enlarged. 

Then  upon  resorting  to  auscultation  I  at  once  distinguished  a 
diastolic  murmur,  which  was  located  at  the  left  of  the  sternum  in 
the  third  interspace,  was  transmitted  downward,  and  possessed 
the  peculiar  quality  of  the  aortic  regurgitant  bruit  (Fig.  76). 
This  was  quite  naturally  taken  to  be  aortic,  until  pondering  on 


Fig.    76.  —  Area    of    Maximum    Intensity 

(.SMALL    CIRCLEj    AND    OF    PkOPAGATION    OF 

Murmur  in  Case  of  Pulmonary  Kegur- 
GITATION   (p.  368). 


370  DISEASES  OF  THE   HEART 

the  size  of  the  right  ventricle  and  the  smallness  of  the  pulse  with- 
out any  suggestion  of  a  collapsing  character  or  of  other  vascular 
signs  of  aortic  incompetence,  the  conviction  was  at  length  forced 
upon  me  that  I  had  to  do  with  pulmonary  regurgitation  pure  and 
simple. 

I  may  add  that  both  sounds  at  the  apex  were  clear,  while  both 
second  sounds  at  the  base  were  feeble,  and  both  heart-tones  were 
audible  in  the  cervical  arteries.  If  secondary  tricuspid  insuffi- 
ciency existed,  it  was  not  recognised.  I  do  not  believe  it  was  pres- 
ent, but  that  the  enormous  hypertrophy  of  the  right  ventricular 
wall  prevented  such  a  degree  of  dilatation  as  would  have  been 
necessary  to  set  up  tricuspid  regurgitation. 

Not  being  able  to  relieve  this  patient's  sense  of  weakness,  nerv- 
ousness, and  inability  to  take  sufficient  food,  and  above  all  to  quiet 
the  violent  action  of  the  heart,  all  of  which  constituted  her  symp- 
toms, I  was  not  called  in  often,  and  after  a  few  weeks  was  notified 
of  her  death,  as  nearly  as  could  be  determined,  from  exhaustion. 

Here  was  a  patient  w^ho  to  her  certain  knowledge  had  been 
the  subject  of  some  form  of  heart-disease  for  fifty  years,  a  fact  in 
itself  highly  interesting  and  unusual.  Moreover,  it  had  not  inca- 
pacitated her  for  attending  to  all  the  duties  of  a  housekeeper  and 
mother  of  eight  children.  And  lastly,  when  the  physical  signs 
were  carefully  determined,  they  were  found  to  indicate  regurgi- 
tation into  the  right  and  not  the  left  ventricle,  consequently  pul- 
monary regurgitation.  As  no  definite  and  reliable  history  of  dis- 
eases in  childhood  and  infancy  could  be  obtained,  I  was  unable 
to  decide  whether  hers  was  a  congenital  or  an  acquired  lesion.  It 
seems  to  me  that  there  is  much  matter  for  reflection  in  the  history 
of  this  case  and  in  the  long  delay  of  symptoms,  which  were  those 
of  increasing  venous  stasis,  without,  however,  any  complaint  of 
dyspnfpa.  It  would  seem  to  indicate  that  if  this  disease  is  unat- 
tended by  stenosis,  there  are  no  symptoms  so  long  as  compensation 
is  maintained,  and  that  this  is  capable  of  being  preserved  for  many 
years. 

Physical  Signs. — The  diagnosis  of  pulmonary  regurgitation 
concerns  both  the  secondary  and  the  primary  form.  The  former, 
it  will  be  recollected,  is  a  relative  insufficiency  depending  upon 
some  antecedent  pulmonary  or  cardiac  disease,  and  therefore  its 
physical  signs  are  likely  to  be  obscured  by  those  of  the  associated 


PULMONARY   REGURGITATION  371 

affection.  The  possibility  of  its  occurrence  in  the  late  stages  of 
mitral  or  aortic  disease  should  always  be  borne  in  mind,  and  if  in 
such  a  case  a  diastolic  murmur  develops  in  the  pulmonic  area,  the 
diagnosis  of  secondary  pulmonary  incompetence  may  be  assumed. 
Particulars  regarding  this  murmur  will  be  considered  under  the 
head  of  auscultation,  to  which,  therefore,  the  reader  is  referred. 

Inspection. — This  discloses  nothing  characteristic  in  the  sec- 
ondary form,  the  evidences  of  circulatory  embarrassment  being  due 
to  the  associated  affections.  Even  in  the  primary  form  the  exist- 
ence of  visible  signs  of  heart-disease  is  likely  to  depend  upon  its 
severity.  So  long  as  compensation  is  preserved,  inspection  of  the 
prsecordia  detects  nothing  more  than  a  forcible  and  perhaps  ex- 
tended cardiac  impulse,  which,  to  judge  from  the  case  I  have 
briefly  reported,  is  particularly  pronounced  in  the  epigastrium. 
So  soon,  however,  as  the  right  ventricle  begins  to  fail  ocular  signs 
of  venous  stasis  appear,  of  the  same  character  as  in  other  cardiac 
affections. 

Palpation. — This  is  of  considerable  service  in  the  detection  of 
the  right  ventricle  hypertrophy  and  in  the  study  of  the  pulse. 
Pulsation  in  the  epigastrium  is  forcible  and  imparts  to  the  palpat- 
ing hand  the  impression  of  a  powerfully  contracting  ventricle.  It 
is  in  the  study  of  the  peripheral  arteries  that  palpation  is  of 
greatest  value. 

Inasmuch  as  the  murmur  is  so  closely  like  that  of  aortic  regur- 
gitation as  to  often  leave  one  in  doubt  concerning  its  real  signifi- 
cance, the  pulse  must  be  relied  on  for  differential  information. 
In  pulmonary  incompetence  the  aortic  system  does  not  experience 
the  sudden  distention  and  equally  rapid  collapse  of  aortic  insuf- 
ficiency, and  consequently  the  pulse  is  not  at  all  like  that  de- 
scribed by  the  term  collapsing.  On  the  contrary,  it  is  likely  to  be 
small  and  weak,  presenting  in  this  respect  a  striking  contrast  to 
what  might  be  looked  for  in  connection  with  the  diastolic  murmur 
at  the  base  of  the  heart. 

The  rate  and  rhythm  of  the  pulse  are  determined  by  the  state 
of  compensation.  If  one  could  place  his  finger  on  the  pulmonary 
artery  he  would  discover  that  this  vessel  and  not  the  aorta  under- 
goes forcible  distention  and  sudden  collapse. 

Percussion. — Pulmonary  regurgitation  affects  the  size  of  the 
right  ventricle,  and  consequently  the  area  of  cardiac  dulness  is 


372  DISEASES  OF   THE  HEART 

increased,  chiefly  doAvnward,  Avliile  that  at  the  left  is  but  slightly 
if  at  all  changed.  This  means  of  investigation  is  therefore  of  great 
importance  in  enabling  one  to  differentiate  between  pulmonary 
and  aortic  incompetence. 

In  the  relative  form  cardiac  dulness  is  already  augmented  to 
the  right,  and  hence  percussion  is  of  less  value  than  in  the  primary 
variety  of  this  valvular  lesion.  It  may  nev^ertheless  be  of  minor 
aid  in  enabling  one  to  determine  a  degree  of  enlargement  of  the 
right  heart  out  of  proportion  to  what  would  be  expected  did  mitral 
or  aortic  disease  exist  without  pulmonary  leakage. 

Auscultation. — Contrary  to  what  is  usually'  the  case,  and  to 
what  has  been  stated  in  previous  chapters  concerning  the  diagnos- 
tic value  of  this  means  of  examination,  auscultation  is  of  the  great- 
est assistance  in  the  detection  of  this  particular  lesion,  not  only 
because  of  its  recognition  of  a  murmur,  but  also  because  by  it  we 
are  able  to  determine  the  absence  of  those  vascular  phenomena  that 
attend  aortic  disease  of  the  same  nature.  Barie  directs  attention 
to  the  importance  of  carefully  studying  the  pulmonic  second  tone, 
since,  as  he  says,  the  earliest  and  in  some  cases  the  only  evidence 
of  relative  insufficiency  of  these  valves  is  to  be  found  in  a  muffling 
or  impurity  of  this  sound.  Consequently,  if  in  a  given  ease  of 
cardiac  disease,  which  ought  naturally  to  intensify  the  pulmonic 
second  tone,  there  is  heard  instead  an  enfeeblement  and  trifling 
impurity  of  this  sound,  it  should  render  one  suspicious  of  dilata- 
tion of  the  artery  and  consequent  incompetence  of  its  valve. 

If  a  characteristic  murmur  results,  this  is  diastolic  (Fig.  77), 
accompanying  the  second  heart-sound  or  even  replacing  that  usu- 
ally heard  in  the  second  left  interspace.  In  primary  lesions  this 
murmur  is  probably  always  present,  and  when  stenosis  is  com- 
bined there  is  also  a  pulmonic  systolic  murmur,  so  that  there  is  a 
double  or  to-and-fro  bruit,  the  same  as  when  there  is  regurgitation 
at  the  aortic  orifice.  The  seat  of  mnxinium  intensity  of  this  dias- 
tolic murmur  is  at  the  left  of  the  sternum  in  the  second  and  third 
left  interspaces.  Its  direction  of  transmission  is  downward  along 
the  left  sternal  margin,  and  its  quality  is  soft.  Indeed,  it  may  so 
closely  agree  with  all  the  characters  of  an  aortic  regurgitant  bruit 
as  to  make  it  absolutely  essential  that  one  study  carefully  all  the 
secondary  signs  before  he  can  arrive  at  a  differential  diagnosis. 
It  should  be  remembered,  liowover,  that  the  pulmonic  murmur  is 


PULMONARY*  REGURGITATION 


373 


not  heard  at  the  right  of  the  sternum,  as  is  generally  the  aortic. 
Yet  this  is  not  alone  sufficient  for  its  recognition,  since  an  aortic 
diastolic  murmur  is  sometimes  inaudible  at  the  right  and  audible 
at  the  left  of  the  breastbone.     Should  a  pulmonic  systolic  murmur 


Fig.  77. — Rhythm  of  Murmur  in  Ttpical  Case  of  Pulmonary  Eegurgitation. 


be  associated,  this  is  not  transmitted  into  the  arteries  of  the  neck, 
but  instead  the  ordinary  heart-sounds  are  there  audible,  a  circum- 
stance which  is  of  diagnostic  aid. 

Diagnosis. — The  difficulty  which  attends  the  diagnosis  of  this 
affection  consists  not  in  the  recognition  of  the  murmur,  but  in  its 
interpretation,  since  it  is  likely  to  be  mistaken  for  the  bruit  of 
aortic  regurgitation.  It  is  indispensable,  therefore,  to  pay  atten- 
tion to  the  secondary  signs,  of  which  the  most  valuable  are  those 
connected  with  the  vascular  system.  For  the  reasons  stated  under 
palpation,  there  can  be  no  acoustic  phenomena  connected  with  the 
arterial  system  in  pulmonary  insufficiency;  and  consequently  the 
absence  of  a  systolic  snap,  and  still  more  of  the  double  souffle  in 
the  femorals,  would,  in  conjunction  with  hypertrophy  of  the  right, 
not  the  left  ventricle,  and  with  a  diastolic  murmur  at  the  left  car- 
diac base,  enable  one  to  state  quite  positively  that  the  regurgita- 
tion was  at  the  pulmonic,  not  the  aortic  ostium.  The  foregoing 
remark  applies  to  the  relative  as  well  as  the  primary  lesion ;  for 
even  in  cases  of  combined  aortic  and  mitral  incompetence,  careful 
study  of  the  peripheral  arteries  detects  some  of  the  characteristic 


374  DISEASES  OF  THE  HEART 

signs  of  the  former  condition.  When,  on  the  contrary,  mitral  dis- 
ease has  led  to  pulmonary  insufficiency,  such  vascular  evidence  is 
wanting. 

If  the  pulmonic  valve  becomes  relatively  incompetent  in  the 
last  stages  of  aortic  stenosis  (as  I  believe  occurred  in  my  patient 
with  aortic  obstruction  whose  case  was  narrated  in  the  chapter  on 
that  disease),  the  recognition  of  the  secondary  defect  is  very  diffi- 
cult. This  is  so  partly  because  its  murmur  is  faint  and  likely  to 
be  overlooked,  but  also  because  if  detected  it  is  apt  to  be  attrib- 
uted to  a  leak  set  up  for  some  reason  at  the  aortic  orifice.  In  the 
case  of  the  lady  just  alluded  to  such  a  diastolic  bruit  developed 
some  months  prior  to  death,  and  became  attended  by  distressing 
and  at  times  violent  palpitation  at  the  pit  of  the  stomach,  the 
throbbing  being  visible.  Reflection  has  since  convinced  me  that 
this  exaggerated  action  of  the  right  ventricle  was  an  indication  of 
its  hypertrophy,  and  hence  corroborative  of  pulmonary  regurgita- 
tion. I  believe  such  an  observation  might  be  utilized  in  the  future 
diagnosis  of  this  lesion. 

Prognosis. — Very  little  needs  to  be  said  upon  this  subject. 
Xot  only  is  the  disease  incurable,  but  it  is  not  amenable  to  treat- 
ment. In  relative  pulmonary  regurgitation  there  is  already  pres- 
ent a  disease  that  affords  a  grave  prognosis,  else  the  pulmonic  valve 
would  not  give  way,  and  the  addition  of  this  complication  serves 
to  hasten  the  downward  progress  of  the  patient.  It  shows  that  the 
original  affection  has  reached  an  extreme  stage,  and  that  the  right 
ventricle  will  not  long  be  able  to  withstand  the  strain. 

If  the  pulmonary  incompetence  is  unattended  by  other  cardiac 
disease,  and  if  compensatory  hypertrophy  is  good,  the  lesion  being 
discovered  accidentally  perhaps,  the  regurgitation  may  last  for 
years  without  producing  serious  circulatory  disturbance,  as  shown 
by  my  patient  who  had  the  lesion  fifty  years.  This  freedom  from 
symptoms  is  the  exception,  however,  for  the  wall  of  the  right  ven- 
tricle is  so  thin  that  compensatory  hypertrophy  is  likely  to  be 
easily  ruptured,  and  when  subjective  symptoms  once  set  in  they 
are  likely  to  be  progressive.  The  occurrence  of  albuminuria  and 
dropsy  is  to  be  regarded  as  of  very  evil  import  and  to  betoken  the 
not  vci'v  rcinotc  tcnninalion  of  ''c  case. 

Mode  and  Causes  of  De^  .. — Baric  speaks  of  the  occur- 
rence of  pulmonary  embolisms  ;        not  remote  contingency  and  as 


PULMONARY  REGURGITATION  3Y5 

contributing  to  the  patient's  death.  The  fatal  termination  is 
most  likely  to  supervene  slowly,  in  consequence  of  cardiac  or  gen- 
eral exhaustion,  rather  than  suddenly,  and  yet  this  latter  event  is 
not  impossible.  Congenital  cases,  particularly  if  combined  with 
stenosis,  may  lead  to  pulmonary  phthisis  through  anaemia  of  the 
lungs. 


CHAPTER    XIII 
PULMONARY    STENOSIS 

This  is  an  obstructive  lesion  which  in  its  effect  on  the  right 
ventricle  is  analogous  to  that  of  aortic  stenosis  on  the  left.  It  dif- 
fers from  the  latter,  however,  in  its  origin  and  anatomical  char- 
acters. It  is  divided  into  two  great  classes,  the  congenital  and  the 
acquired,  the  former  constituting  bv  far  the  greater  number.  Even 
when  congenital,  this  lesion  is  one  of  the  rare  forms  of  heart- 
disease.  Instances  of  the  acquired  affection  are  so  extremely  in- 
frequent that  since  Constantin  Paul's  elaborate  monograph  in 
1871  only  8  cases  have,  so  far  as  I  know,  been  reported.  For  my 
knowledge  of  these  cases  I  am  indebted  to  a  thesis  by  Koehler,  of 
Halle,  in  1894.  I  have  not  been  able  to  ascertain  how  many 
of  the  cases  described  by  Paul  belong  to  each  variety.  The 
3  cases  reported  in  189.5  by  Boviard,  Holt,  and  Forlanini, 
and  the  3  in  189G  by  Adams,  Arnozan,  and  Siredy,  all  appear 
to  have  been  congenital,  which  still  further  emphasizes  the 
rarity  of  the  acquired  form.  The  first  case  on  record  of  this 
form  was  described  in  the  Atlas  of  Pathological  Anatomy  by 
Cruveilhier. 

Morbid  Anatomy. — This  can  be  best  described  by  the  repe- 
tition of  a  report  of  the  8  cases  above  alluded  to,  which  was  pub- 
lished by  me  in  the  Journal  of  Medicine  in  January,  1897. 

In  1873  the  late  Christian  Fenger  pul)lished  a  case  in  a  male 
of  nineteen  years  in  wliich  the  disease  was  traceable  to  an  attack 
of  articular  rheumatism  at  the  age  of  eleven.  The  autopsy  dis- 
closed numerous  vegetations  attached  to  the  pulmonary  valve  and 
along  the  wall  of  the  artery  as  far  as  its  bifurcation  and  into  its 
main  branches,  particularly  the  left.  This  condition,  although  the 
vessel  was  dilated,  had  led  to  very  great  obstruction,  with  consecu- 
tive hypertrophy  of  the  right  ventricle.  The  septa  were  intact,  the 
pulmonary  artery  and  its  main  right  branch  dilated.  Fenger, 
376 


PULMONARY  STENOSIS  377 

from  the  history  and  post-mortem  discovery  of  recent  endocarditis, 
concluded  that  there  could  be  no  doubt  of  the  postnatal  origin  of 
this  case. 

Moritz  Mayer  next  reported  a  case  in  IS 74  in  a  girl  of  sixteen, 
who  at  the  age  of  eleven  had  suffered  from  some  pulmonary  dis- 
ease and  from  endocarditis.  The  necropsy  revealed  cauliflower 
vegetations  attached  to  the  wall  of  the  conus  arteriosus  and  to  the 
pulmonary  valves,  with  secondary  hypertrophy  and  dilatation  of 
the  right  ventricle.  The  ductus  arteriosus  was  closed,  but  the 
interventricular  sieptum  contained  an  opening  large  enough  to 
admit  the  tip  of  the  first  finger,  and  Mayer  explained  this  defect 
as  having  originated  after  birth  in  consequence  of  the  previous 
endocarditis. 

Rinsenna's  case  in  1883  was  in  a  patient  aged  thirty-four,  who 
had  also  had  acute  rheumatism.  On  post-mortem  examination  the 
pulmonary  valves  were  found  greatly  thickened,  and  to  have  thus 
caused  slight  obstruction,  but  without  enlargement,  of  the  right 
ventricle. 

In  1884  Krannhals  reported  2  cases,  of  which  one  was  in  a 
widow  of  forty-three  suffering  from  leuctemia,  and  the  pulmonary 
stenosis  was  attributed  to  this  affection.  Neither  necrosis  of  the 
valves  nor  micro-organisms  were  found  to  explain  the  stenosis. 
In  his  second  case,  that  of  a  housemaid  of  nineteen,  there  was  a 
history  of  good  health  up  to  the  fourth  year,  when  she  had  an 
attack  of  rheumatism,  and  her  health  had  been  impaired  since  that 
time.  The  foetal  passages  were  found  closed,  there  were  no  con- 
genital defects,  but  the  pulmonary  artery  was  dilated. 

Rendu  in  1884  described  a  case  in  a  girl  of  nineteen,  who  had 
had  the  disease  for  fifteen  years,  and  after  death  the  pulmonary 
valves  were  found  fused  into  an  inflexible  diaphragm  having  an 
opening  of  about  xV  of  an  inch  in  diameter.  The  immediate  cause 
of  death  was  a  rapidly  progressing  nephritis. 

Stybr's  case  in  1890  was  that  of  a  woman  of  twenty-four  in 

whom  the  stenosis  was  found  due  to  an  inflammatory  blending 

of  the  pulmonary  segments  into  a  tendon-like  cone  that  projected 

into  the  lumen  of  the  artery  and  contained  at  its  apex  an  opening 

2  millimetres  in  wadth.     Two  oblique  lines  that  passed  down  the 

sides  of  the  cone  showed  where  the  cusps  had  become  united.     The 

right  ventricle  was  enormously  hypertrophied.    As  the  aortic  cusps 
26 


378  DISEASES  OP  THE   HEART 

were  slightly  sclerosed,  Koeliler  thinks  the  inllainniatory  process 
must  have  dated  from  intra-uterine  life. 

Finally,  Koehler  described  the  ease  of  a  housemaid  of  twenty- 
one  who  was  admitted  to  the  hospital  in  July,  1893,  suffering  from 
pneumonia,  and  who  gave  a  history  of  acute  rheumatism  the  May 
previous.  Since  that  time  her  health  had  been  poor,  and  she  had 
suffered  from  dyspud-a.  The  autopsy  disclosed  i^olypoid  vegeta- 
tions springing  from  the  wall  of  the  pulmonary  artery  in  such  a 
manner  as  to  prevent  the  complete  opening  of  the  valve  during 
ventricular  systole.  The  valve-segments  as  well  as  the  endocar- 
dium of  the  right  ventricle  were  healthy,  but  similar  vegetations 
were  found  in  the  aorta  so  disposed  as  to  prevent  the  adequate 
opening  of  these  valves,  and  to  thus  cause  a  stenosis  of  this  orifice, 
the  same  as  on  the  right  side.  Both  ventricles,  j)articularly  the 
right,  were  dilated.  The  Sieptum  was  intact  and  the  foramen  ovale 
was  closed. 

In  the  foregoing  cases,  with  exception  of  Rendu's  and  Stybr's, 
there  were  evidences  of  recent  endocarditis,  absence  of  congenital 
abnormalities,  and  dilatation,  or  at  least  no  perceptible  narrowing, 
of  the  pulmonary  artery.  Acquired  cases  present  striking  differ- 
ences from  most  of  the  congenital  in  their  pathological  appear- 
ances, but  they  both  have  the  common  feature  of  hypertrophy  and 
dilatation  of  the  right  ventricle. 

In  the  congenital  form  the  obstruction  is  due  most  usually  to  a 
fusing  together  of  the  valve-segments,  which  then  form  either  a 
diaphragm  stretching  across  the  ostium  or  a  cone-like  projection 
into  the  artery  with  a  small  opening  at  its  apex  (Fig.  78).  The 
foramen  ovale  is  usually  open,  and  the  interventricular  steptum  is 
sometimes  incom])lete.  The  pulmonary  artery  is  always  nar- 
rowed, and  there  may  be  atresia  of  this  vessel.  The  ductus  arterio- 
sus is  generally  oi)en,  yet  is  in  some  cases  found  closed.  Very 
rarely  the  stenosis  is  caused  by  constriction  of  the  right  conus 
arteriosus,  in  which  event  this  may  appear  like  a  third  ventricle, 
and  both  the  interventricular  and  interauricular  septa  are  defect- 
ive, the  pulmonary  artery  is  narrowed  or  even  occluded,  and  the 
ductus  Botalli  remains  pervious. 

In  other  cases  there  are  various  errors  of  development,  as  trans- 
position of  the  aorta  and  pulmonary  artery,  or  their  origin  from 
one  common  tnmk ;  a  blending  of  the  two  ventricles  into  one  com- 


PULMO^fARY   STENOSIS 


379 


mon  cavity  with  but  one  instead  of  two  auricles ;  or  one  ventricle 
and  two  auricles,  or  but  one  auricle  and  two  ventricles. 

It  is  not  always  easy  to  determine  post  mortem  whether  a  given 
case  belongs  to  the  congenital  or  the  acquired  category.     In  well- 


**.. 


Fig.  78. — Heart  of  a  Boy,  showing  Congenital  Stenosis  of  the  Pulmonary  Orifice. 
Specimen  in  collection  of  Dr.  Gustav  Filtterer. 


marked  specimens,  like  Fenger's,  or  in  such  as  show  striking  ab- 
normalities of  development  the  decision  may  be  easy ;  but  in  cases 
presenting  some  of  the  characteristics  of  both  forms  the  exact 
nature  must  be  left  in  doubt. 

Aside  from  the  evidences  of  recent  endocarditis  it  is  the  condi- 
tion of  the  pulmonary  artery  upon  which  pathologists  rely  for  the 
determination  of  the  intra-  or  extra-uterine  development  of  the 


380  DISEASES  OF  THE   HEART 

lesion.  Dilatation  of  this  vessel  makes  strongly  for  the  acquired 
form,  while  narrowing  of  the  artery  points  to  the  foetal  origin  of 
the  disease. 

Etiology. — The  congenital  form  can  be  dismissed  with  the 
statement  that  it  results  either  from  intra-uterine  endocarditis  or 
myocarditis,  or  from  defective  development. 

Acquired  cases  also  originate  in  endocarditis  either  of  rheu- 
matic causation  or  in  the  course  of  other  acute  infectious  processes, 
as  shown  in  the  histories  of  the  8  cases  above  narrated.  Its  rarity 
is  due  to  the  fact  that  after  birth  the  right  heart  is  seldom  the  seat 
of  acute  inflammation. 

In  a  ninth  case  that  has  come  to  my  notice,  that  of  A.  Kasem- 
Bek  in  1899,  the  pulmonary  stenosis  was  caused  by  a  gumma  on 
the  ostium. 

Symptoms. — These  depend  largely  upon  the  congenital  or 
acquired  nature  of  each  case.  Moreover,  in  the  latter  the  clinical 
history  is  also  influenced  by  the  presence  or  absence  of  acute  endo- 
carditis. If  the  cases  are  not  stumbled  upon  accidentally  in  the 
course  of  examination  or  treatment  for  some  other  wholly  differ- 
ent disease,  the  patients  are  likely  to  be  seen  when  the  affection  has 
led  to  pronounced  disturbance  of  the  general  health.  In  such  there 
are  dyspnoea  and  other  ordinary  evidences  of  cardiac  asthenia,  or 
there  is  a  complaint  of  vague  general  distress  and  ill  health.  In 
a  word,  there  are  no  symptoms  peculiar  to  pulmonary  stenosis  as 
contrasted  with  other  valvular  lesions. 

In  the  congenital  form  patients  are  apt  to  be  weakly,  under- 
sized, sometimes  mentally  deficient,  and  to  manifest  striking  cya- 
nosis. This  is  not  always  present,  however.  In  the  chapter  on 
Congenital  Cardiac  Affections  will  also  be  considered  certain 
changes  in  the  blood  that  accompany  marked  cyanosis  or  the  Mor- 
bus Ceruleus  of  older  writers. 

Sufferers  from  juilmonary  stenosis  are  very  apt  to  die  from 
tuberculosis  of  the  lungs,  as  is  sho^vn  in  the  only  instance  of  this 
cardiac  disease  I  have  observed,  and  which  was  published  in  my 
paper  previously  mentioned.  A  plumber's  helper,  aged  twenty- 
three,  was  first  seen  by  me  at  my  clinic  at  Cook  County  Hospital, 
having  been  sent  from  Ward  4  as  a  case  of  pulmonary  tuberculosis. 
Family  history  was  meagre.  His  father  had  died  of  some  wast- 
ing disease  with  cough ;  his  mother  of  cancer ;  two  sisters  living 


PULMONARY  STENOSIS 


181 


and  healthy.  Patient  declared  he  was  healthy  in  infancy  and 
childhood,  and  had  never  snffered  from  dyspnoea  on  exertion 
prior  to  his  present  illness, 
and  had  not  exhibited  c^^a- 
nosis.  In  fact  he  was  healthy 
nntil  his  present  illness  began 
three  months  before  his  ad- 
mission to  the  hospital. 

Withont  entering  too  much 


into  detail,  it  will  suffice  to 
state  that  he  presented  the 
usual  symptoms  of  consump- 
tion, emaciation,  cough,  pro- 
fuse muco-purulent  exj)ectora- 
tion,  febrile  temperature,  and 
a  rapid,  feeble  pulse,  the  func- 
tions of  the  digestive  organs 
ig   good. 


Fig.  79. — Relative  Cardiac  Dulness  in 
Case  of  Pulmonaky  Stenosis  (p.  380). 


remaining   good.      There    was 

no  cyanosis.     The  right  apex 

was    retracted,    and    expanded    poorly    upon    inspiration.      Both 

apices  showed  dulness,  bronchial  breathing,  and  moist  rales. 

The  prsecordium  bulged 
from  the  third  rib  to  the  epi- 
gastrium and  from  left  to 
right  nipple.  There  was  a 
short,  weak  systolic  thrill  in 
second  left  interspace,  1  inch 
from  sternum.  Absolute  dul- 
ness was  increased  from  the 
level  of  the  second  costal  carti- 
lage to  the  lower  border  of  the 
fifth  rib,  and  from  1^  inch  to 
right  of  sternum  to  ^  inch  in- 
side of  left  mamillary  line 
(Fig.  79). 

The  heart's  rhythm  was 
regular    and    accelerated,    the 

FiG^SO.-LccATioN  OF  Thrill  AND  Systolic       ^^^^^^^   ^^-         ^.g^,^,    ^^^^^       ^^^ 
Murmur  in  Case  of  Pulmonary  Steno-  ~  '  ' 

SIS  (p.  380).  first  muffled  and  dull,  while  the 


382  DISEASES   OF  THE    HEART 

second,  in  the  third  left  interspace,  was  short,  high-pitched,  and  so 
feeble  as  to  be  rndimentary.  A  harsh  systolic  murmur  was  audible, 
having  its  maximum  intensity  in  the  second  left  interspace,  1  inch 
from  sternum,  and  corresponding  in  position  to  the  soft  systolic 
thrill  previously  mentioned  (Fig.  SO).  It  was  transmitted  with 
special  clearness  upward  and  outward  towards  the  left  shoulder 
and  around  the  left  side  to  the  l)ack,  but  could  be  distinguished 
feebly  even  in  the  right  half  of  the  thorax.  The  liver  was  not 
appreciably  enlarged.  Tubercle  bacilli  were  discovered  in  the 
sputum. 

The  diagnosis  was  made  of  pulmonary  stenosis  \vith  secondary 
hypertrophy  and  dilatation  of  the  right  ventricle ;  tuberculosis  of 
both  lungs  and  moderate  venous  and  visceral  congestion  consecu- 
tive to  the  cardiac  lesion.  This  was  thought  to  be  congenital, 
although  there  was  no  history  of  cyanosis  in  infancy,  and  no  evi- 
dence of  other  congenital  cardiac  defects.  The  patient  was  kept 
under  observation  until  January  10,  189G,  when  he  was  found 
dead  in  his  bed.  Symptoms  of  general  asthenia  increased  in  sever- 
ity, and  diarrhoea  set  in  a  day  or  two  before  death. 

j^ecropsy  was  made  by  Dr.  F.  Tice  twenty-four  hours  after 
death.  The  lung-tindings,  l)riefly  stated,  were  those  of  pulmonary 
tuberculosis.  The  pericardium  contained  from  one  and  a  half  to 
two  ounces  of  fluid.  Aorta  was  not  enlarged;  the  pulmonary 
artery  was  larger  than  the  aorta,  dilatation  extending  into  the  two 
branches,  the  left  more  than  the  right.  The  aortic  valves  were 
found  competent,  l>ut  the  pulnmnarv  valves  leaked  slowly  to  the 
hydrostatic  test. 

Looking  into  the  j)iihiionarv  artery  from  above,  it  appeared 
as  if  a  nipple  with  a  small  opening  at  its  apex  projected  into  the 
vessel,  and  at  one  side  near  its  base  was  a  second  small  opening, 
which  was  closed  in  below  by  a  thinner  membrane  (Fig.  81).  The 
right  ventricle  was  hypertrophied  and  dilated,  and  the  right  auri- 
cle was  also  enlarged.  One  cusp  of  the  tricuspid  valve  showed  a 
slight  thickening  ahmg  its  base.  The  mitral  valves  were  negative 
except  a  slight  thickening;  aortic  valves  were  thickened  along  base 
and  margins,  while  small  atheromatous  phupies  were  found  in  the 
beginning  of  the  aorta. 

The  left  ventricle  appeared  slightly  dilated.  The  interven- 
tricular sa;'ptum  was  complete,  but  in  the  interauricular  Sfcptum 


PULMONARY  STENOSIS 


383 


there  was  a  valve-like  passage,  which  would  not  quite  admit  two 
matches,  was  perhaps  3  millimetres  in  diiimeter,  and  corresponded 


Fig.  81. — Heart  from  Case  of  Pulmonary  Stenosis  (p.  380). 
Line  shows  narrowed  pulmonary  orifice. 

in  situation  and  shape  to  the  foramen  ovale  (Fig.  82).  Thus  it 
was  seen  that  the  intra-vitam  diagnosis  was  confirmed  in  its  main 
features.  A  more  careful  inspection  of  the  heart,  made  a  year 
later  after  having  been  preserved  in  a  formalin  solution,  showed 
that  the  cone  which  projected  into  the  pulmonary  artery,  and  rep- 
resented the  semilunar  valves,  was  made  up  of  a  uniform  mem- 
brane, somewhat  thicker  than  normal  valves,  and  showed  no  lines 
or  ridges  that  indicated  the  points  of  fusion  of  the  cusps.  The 
opening  at  the  apex  was  oval,  measuring  15  millimetres  by  8  milli- 
metres at  its  broadest  point.  The  edges  of  the  cone  were  thick- 
ened, and  the  second  minute  opening  at  its  side,  near  its  base,  was 


384 


DISEASES  OF  THE  HEART 


found  to  be  a  saccular  dilatation  projecting  into  the  Inmen  of  the 
cone.  The  diameter  of  the  pnlnionarv  artery  was  22  millimetres, 
of  the  aorta  18,  and  of  the  foramen  ovale  3  millimetres. 

From  the  foregoing  description  it  is  apparent  with  what  imcer- 
taintv  one  can  classify  this  case  as  congenital  or  acquired.  There 
were  no  indications  of  endocarditis,  as  it  ordinarily  appears  after 


Fi(i.  !s'.i. — Same  IIeakt  as  Fig.  81. 
Left  iiuricle  is  laid  open,  und  line  indicates  patent  foramen  ovale. 

birth.  The  pulmonary  artery  was  not  contracted,  but  rather 
dilated,  the  interventricular  sa'ptum  was  complete,  and  the  fora- 
men ovale  was  not  more  patent  than  it  is  in  a  considerable  propor- 
tion of  hearts  without  a  suspicion  of  congenital  disease.  Never- 
theless, the  appearance  of  the  cone,  which  replaced  the  semilunar 


PULMONARY  STENOSIS  385 

valves,  rendered  it  probable  that  this  case  was  of  congenital  origin, 
and  that  intra-nterine  endocarditis  caused  a  fusion  of  the  seg- 
ments at  a  period  subsequent  to  the  closure  of  the  septa,  and 
that  the  stenosis  was  not  sufficient  to  prevent  the  closure  of 
the  foramen  ovale  after  birth.  Moreover,  the  volume  of  blood 
driven  into  the  j^ulmonary  artery  could  not  have  been  very  small, 
and  must  have  been  divided  into  fluid  veins,  which  threw  the 
stream  against  the  arterial  coats  in  such  a  way  as  to  maintain  ade- 
quate blood-pressure  within  the  vessel.  It  is  interesting  to  reflect 
that,  although  the  lesion,  according  to  the  patient's  history,  gave 
rise  to  no  subjective  symptoms,  it  should  yet  ultimately  have  led 
to  pulmonary  tuberculosis,  the  usual  sequence  in  such  cases. 

Regarding  physical  signs  in  this  case,  it  is  also  of  interest  to 
note  the  wide  propagation  of  the  murmur.  This  was  more  marked 
in  the  left  lung,  and  as  the  left  branch  of  the  pulmonary  artery 
was  found  to  be  rather  larger  than  the  right,  there  was  probably 
direct  connection  between  the  size  of  the  artery  and  the  transmis- 
sion of  the  murmur ;  for  had  the  vessel  been  narrowed,  the  audi- 
ble vibrations  could  not  have  been  transmitted  to  any  great  dis- 
tance. 

If  a  conclusion  from  a  single  case  is  justifiable,  it  is  likely  that 
the  symptoms  directly  referable  to  pulmonary  stenosis  depend 
upon  its  degree  and  upon  the  association  of  other  developmental 
defects  even  more  than  upon  the  obstruction  itself. 

Physical  Signs. — Inspection. — Cyanosis  is  not  always  pres- 
ent in  congenital  cases,  and  when  present  is  not  uniform  thro.ugh- 
out  the  body.  It  is  this  bluish  tint  which  led  old  writers  to  des- 
ignate the  underlying  abnormality  by  the  generic  term  of  Morbus 
Ceruleus.  Cyanosis  is  most  apparent  on  the  cheeks,  ears,  fingers, 
elbows,  and  knees,  and  is  intensified  by  coughing  or  physical  exer- 
tion. As  shown  by  my  case,  it  is  not  so  likely  to  be  present  when 
the  stenosis  has  not  led  to  or  is  not  associated  with  defects,  as,  e.  g., 
patency  of  the  foramen  ovale  or  of  the  interventricular  sseptum. 

In  the  acquired  form  patients  are  more  apt  to  show  pallor  of 
the  countenance,  and  there  may  be  turgescence  of  the  superficial 
veins  as  a  direct  result  of  interference  with  the  outflow  of  blood 
from  the  right  heart.  Inspection  of  the  prsecordium  detects  bulg- 
ing over  the  situation  of  the  right  ventricle — i.  e.,  at  the  lower  end 
of  the  sternum  and  the  parts  immediately  adjacent.     Such  a  bulg- 


386  DISEASES  OF  THE   HEART 

ing  is  most  marked  in  cases  in  which  the  valvular  lesion  is  either 
congenital  or  has  existed  from  very  tender  years.  It  is  due  to 
hypertrophy  of  the  right  ventricle,  and  hence  there  is  associated 
pulsation  in  the  epigastrium  and  over  the  prominent  area. 

PaJpation. — This  corroborates  some  of  the  information  de- 
rived by  inspection,  and  enables  one  still  better  to  appreciate  the 
extent  and  force  of  the  cardiac  impulse  imparted  by  the  hyper- 
trophied  right  ventricle.  In  addition,  there  is  usually  felt  a  sys- 
tolic purring  vibration  or  thrill  in  the  pulmonic  area — i.  e.,  in  the 
second  left  intercostal  space,  close  to  the  sternum.  This  fremisse- 
ment  may  be  exceedingly  delicate,  as  in  the  case  observed  by  me, 
or  it  may  be  distinct  and  harsh. 

The  pulse  presents  no  distinctive  characters  aside  from  small- 
ness,  feebleness,  and  increased  frequency. 

Percussion. — By  this  means  is  revealed  marked  increase  of 
both  absolute  and  relative  cardiac  dulness,  the  increase  being 
downward  and  to  the  right,  over  the  situation  of  the  right  ventricle 
and  corresponding  auricle  (Fig.  79).  In  my  case  this  alteration 
of  cardiac  dulness  was  very  pronounced,  and  aided  materially  in 
the  diagnosis  of  the  lesion  by  assuring  me  of  the  existence  of  right 
ventricle  hypertrophy. 

Auscultation. — The  conditions  here  are  favourable  to  the  gen- 
eration of  a  bruit,  and  as  it  is  produced  during  the  passage  of  the 
blood  from  the  right  ventricle  into  the  pulmonary  artery,  the  mur- 
mur is  systolic  (Fig.  83).  Its  seat  of  maximum  intensity  is  over 
the  base  of  the  heart,  at  the  left  of  the  sternum,  in  the  second  and 
third  intercostal  spaces  (Fig.  80).  At  first  this  bruit  may  be 
thought  to  be  aortic  in  origin,  but  if  its  direction  of  propagation  is 
studied  this  will  be  found  to  be  upward  and  to  the  left  towards  the 
left  clavicle  rather  than  to  the  right  and  upward,  as  is  the  case 
with  the  murmur  of  aortic  stenosis.  Another  point' of  difference 
is  that  the  pulmonic  systolic  murmur  is  not  heard  in  the  cervical 
arteries,  where,  on  the  contrary,  the  two  cardiac  tones  are  usually 
distinct.  If  intense,  the  murmur  may  be  heard  throughout  the 
pra.'cordium,  though  in  all  instances  its  area  of  maximum  intensity 
corresponds  with  the  location  of  the  systolic  thrill.  In  my  case  the 
murmur  was  transmitted  widely,  but  was  more  distinct  in  the  left 
than  in  the  right  half  of  the  thorax.  In  auscultating  towards  the 
apex  and  over  the  body  of  the  right  ventricle  the  murmur  grows 


PULMONARY  STENOSIS 


387 


less  intense,  while  the  two  cardiac  sounds  become  more  distinct. 
The  murmur  maj-  be  rough  and  loud,  or  soft  and  faint.  The  pul- 
monic second  sound  is  diminished  in  intensity,  or  may  be  absent 
altogether,  while  the  two  aortic  sounds  are  distinct. 


Fig.  83. — Khythm  of  Typical  Polmonaey  Stenotic  Murmur. 


Diagnosis. — The  difficulty  of  diagnosis  in  this  affection  lies 
in  its  differentiation  from  aortic  stenosis  or  possibly  in  deciding 
whether  the  bruit  may  not  be  accidental,  since  it  is  situated  where 
such  an  accidental  murmur  is  so  often  heard.  If,  however,  proper 
attention  is  paid  to  the  secondary  physical  signs  as  described 
above,  in  particular  to  the  evidence  of  hypertrophy  of  the  right, 
not  of  the  left  ventricle,  one  can  scarcely  fail  to  interpret  the  mur- 
mur correctly.  If  after  such  careful  study  of  all  the  physical 
signs  doubt  is  still  entertained,  the  sphygmograph  will  be  found  of 
service  in  enabling  one  to  differentiate  between  this  lesion  and 
aortic  stenosis,  for  it  goes  without  saying  that  pulmonary  obstruc- 
tion can  in  nowise  modify  the  characters  of  the  radial  pulse. 
Finally,  the  discovery  of  pulmonary  tuberculosis  and  of  cyanosis 
in  cases  in  which  the  two  halves  of  the  heart  communicate,  fur- 
nishes a  certain  degree  of  evidence  in  favour  of  the  existence  of 
pulmonary  obstruction. 

Prognosis. — Patients  with  pulmonary  stenosis  rarely  live  be- 
yond the  third  decade.  Even  when  the  disease  does  not  directly 
destroy  life,  it  does  so  indirectly  by  predisposing  to  pulmonary 


388  DISEASES  OF  THE  HEART 

tuberculosis.  This  has  been  so  frequently  observed  that  no  doubt 
can  be  entertained  concerning  the  intimate  connection  existing  be- 
tween these  two  diseases.  When  phthisis  has  once  supervened  the 
prognosis  becomes  that  of  the  secondary  affection,  and  since  the 
stenosis  is  irremovable  there  Ciin  be  no  hope  of  the  arrest  of  the 
tuberculosis.  The  influence  of  this  cardiac  defect  upon  the  pro- 
duction of  consumption  is  through  the  ana?mia  of  the  lungs  which 
the  narrowing  of  the  ostium  occasions. 

Mode  and  Causes  of  Death. — In  ITustedt's  G  cases  of  pul- 
monary stenosis  death  was  caused  in  1  case  by  heart  w'eakness,  in 
another  by  miliary  tuberculosis,  and  in  the  4  others  by  phthisis. 


PULMONARY  STENOSIS 


389 


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CHAPTER    XIV 
COMBINED    VALVULAR    LESIONS 

Cheonic  valvular  defects  have  been  dealt  with  singly,  since 
by  so  doing  their  distinctive  individual  features  could  be  brought 
out  more  clearly  and  without  danger  of  confusion.  It  would  be  a 
mistake,  however,  to  consider  these  forms  of  heart-disease  as 
always,  or  indeed  as  generally,  occurring  alone.  As  a  matter  of 
fact  certain  of  them  are  usually  combined,  while  it  is  possible  for 
any  two  or  three,  or  even  for  all  of  them  to  be  united.  The  most 
common  association  is  that  of  both  stenosis  and  regurgitation  at 
the  same  orifice.  Tkus  it  is  comparatively  rare  to  find  aortic 
obstruction  without  also  some  insufficiency,  or  the  reverse,  while 
in  the  same  manner  the  two  mitral  lesions  are  usually  combined  in 
varying  proportions.  Indeed,  a  moment's  reflection  will  convince 
one  that  the  structural  alterations  set  up  by  endocarditis  are  very 
prone  to  result  in  both  incompetence  of  the  valves  and  narrowing 
of  the  ostium,  the  clinical  features  of  each  case  being  determined 
by  the  predominant  lesion. 

This  is  not  all ;  lesions  at  one  orifice  may  be  complicated  by  a 
defect  situated  at  another.  To  be  explicit,  mitral  stenosis  may  be 
combined  with  either  aortic  stenosis  or  regurgitation,  or  both,  and 
the  same  way  with  mitral  insufficiency,  or  a  double  mitral  disease 
may  be  associated  with  either  or  both  of  the  aortic  defects.  Let  us 
now  consider  these  various  combinations  in  detail. 

COMBINED   MITRAL  STENOSIS  AND   REGURGITATION 

As  already  stated,  the  endocarditic  changes  that  lead  to  mitral 
disease  are  very  apt  to  cause  both  constriction  and  insufficiency. 
Extreme  narrowing  is  more  likely  to  exist  alone  than  is  free  re- 
gurgitation, and  yet  even  when  there  is  a  buttonhole  mitral,  it  is 
possible  for  an  insignificant  leak  to  also  occur,  although  the  insuffi- 
ciency may  not  be  declared  by  a  systolic  apex-murmur.  On  the 
nno 


COMBINED  Valvular  lesions  391 

other  hand,  mitral  segments  that  are  too  stiff  to  close  are  quite 
likely  to  depend  in  front  of  the  opening  in  such  a  manner  as  to 
oppose  some  barrier  to  the  free  ingress  of  the  blood  from  the  auri- 
cle. In  children  the  mitral  curtains  are  not  infrequently  so  shriv- 
elled as  to  form  a  mere  fringe  about  the  ring,  and  when  such  is  the 
case  stenosis  is  absent.  In  adults,  particularly  when  the  incom- 
petence is  the  result  of  atheroma,  pure  and  unmixed  regurgitation 
is  the  exception. 

The  effects  on  the  heart  are  essentially  those  of  either  form  of 
mitral  disease  when  existing  alone,  and  yet  the  left  ventricle  and 
left  auricle  manifest  certain  modiiications  depending  upon  the  as- 
sociation of  stenosis  with  incompetence.  The  ventricle  is  neither 
so  dilated  as  in  unmixed  regurgitation,  nor  so  atrophic  as  when 
there  is  extreme  obstruction.  Similarly,  the  left  auricle  is  neither 
so  hypertrophied  as  in  predominating  stenosis,  nor  so  dilated  as  in 
free  regurgitation.  When  conjoined,  the  two  lesions,  therefore, 
exert  a  somewhat  restraining  influence  upon  each  other  as  regards 
the  secondary  effects  on  the  cardiac  cavities  directly  affected.  The 
changes  in  the  right  heart  are  those  incident  to  retarded  pulmo- 
nary circulation,  and  their  extent  depends  upon  which  of  the  two 
lesions  predominates. 

Symptoms. — The  symptoms  depend  upon  the  degree  of  com- 
pensation, and  this  on  whether  the  stenosis  or  the  regurgitation 
is  the  gre^lter.  They  have  been  described  in  considering  the  re- 
spective mitral  defects,  and  do  not  need  to  be  recapitulated. 

Diagnosis. — The  diagnosis  is  as  a  rule  not  difficult,  for 
the  reason  that  the  signs  of  the  two  diseases  are  combined  with 
varying  distinctness  in  different  cases.  The  apex-beat  is  not  so 
displaced  nor  so  forcible  as  in  uncomplicated  regurgitation,  nor,  on 
the  other  hand,  is  it  so  distinctly  thumping  as  in  pure  stenosis, 
but  presents  the  characters  of  both  affections.  There  is  usually  a 
presystolic  thrill  at  the  apex,  but  it  is  less  long  and  less  intense 
than  in  stenosis  alone,  being  commonly  only  a  short  vibration, 
which  seems  to  be  merely  a  prolongation  of  the  apex-shock.  Car- 
diac dulness  is  increased  transversely,  but  chiefly  to  the  right,  and 
the  pulmonic  second  sound  is  accentuated. 

Auscultation  detects  a  combination  of  both  a  presystolic  and  a 
systolic  murmur,  the  latter  being  well  marked  as  a  rule,  and  the 
former  long  and  relatively  pronounced,  or  short  and  difficult  of 


392  DISEASES  OF   THE  HEART 

recognition,  according  to  the  degree  of  narrowing.  I  have  some- 
times found  in  these  cases  that  the  systolic  bruit  is  the  predomi- 
nant one  in  the  erect  position,  while  in  the  dorsal  decubitus  the 
presystolic  murmur  comes  out  more  distinctly.  This  is  the  reverse 
of  what  has  been  stated  as  the  rule  regarding  the  influence  of 
position  upon  the  two  mitral  murmurs  when  uncombined.  I  have 
also  observed  that  often,  when  only  the  presystolic  bruit  is  audible 
directly  at  the  apex,  the  systolic  murmur  can  be  detected  further 
to  the  left  and  on  the  back. 

Prognosis. — The  prognosis  is,  other  things  being  equal, 
rather  more  favourable  when  these  two  conditions  are  united  than 
when  either  exists  alone,  and  I  believe  for  the  reason  that  they 
tend  to  check  each  other. 

MITRAL    STENOSIS    AND    AORTIC    STENOSIS 

This  is  an  exceedingly  serious  combination,  since  at  both  of  the 
left  ostia  there  is  a  mechanical  impediment  to  the  passage  of  blood 
from  the  pulmonary  into  the  aortic  system.  The  left  ventricle  re- 
ceives and  discharges  an  abnormally  small  volume  of  blood,  de- 
pending on  the  degree  of  constriction,  and  hence  is  a  thick-walled 
chamber  of  limited  capacity,  while  in  marked  contrast  are  the 
greatly  hypertroi)hiod  and  dilated  left  auricle  and  right  ventricle. 

Symptoms. — Symptoms  appear  early,  and  are  pronounced  in 
consequence  of  the  great  stasis  within  the  lungs  and  body  gener- 
ally. Cyanosis  and  dyspnea  are  present,  often  in  an  extreme 
degree,  while  engorgement  of  the  abdominal  and  pelvic  organs  is 
shown  by  all  of  its  attendant  phenomena,  both  subjective  and 
objective. 

Diagnosis. — The  pulse  is  small,  weak,  and  slow  or  acceler- 
ated, according  to  the  state  of  compensation.  The  apex-beat  is 
weak  and  preceded  by  a  presystolic  thrill,  unless  indeed  it  be  pro- 
duced by  the  impulse  of  the  hypertrophied  right  ventricle,  when 
it  may  be  diffused  and  quite  strong  between  the  sternum  and  left 
nipple. 

Epigastric  pulsation  and  a  marked  increase  of  absolute  and 
relative  cardiac  dulness  to  the  right  evince  the  secondary  enlarge- 
ment of  the  right  heart.  There  are  heard  a  rough,  low-pitched 
presystolic  murmur  at  or  within  the  apex  and  an  accentuated  pul- 
monic second  sound  indicative  of  the  mitral  lesion,  and  in  addi- 


combined' VALVULAR  LESIONS  393 

tion,  a  harsh  systolic  bruit  in  the  aortic  area  with  a  feeble  second 
tone,  showing  obstruction  at  this  orifice." 

Prognosis. — The  prognosis  is  of  necessity  very  unfavourable, 
since  compensation  cannot  long  be  preserved,  and  when  broken 
can  be  restored,  if  at  all,  only  with  great  difficulty. 

MITRAL    STENOSIS    AND    AORTIC    REGURGITATION 

This  is  also  a  serious  combination,  yet  the  degree  of  its  gravity 
is  determined  by  the  extent  and  predominance  of  the  lesions. 

The  secondary  effects  on  the  heart  are  those  produced  by  ob- 
structed outflow  from  the  kings  and  left  auricle,  together  with 
such  as  are  usually  caused  by  reflux  into  the  left  ventricle — 
namely,  hypertrophy  and  dilatation  of  the  left  auricle  and  right 
ventricle,  and  in  the  case  of  the  left  ventricle,  such  a  degree  of 
hypertrophy  and  dilatation  as  would  follow  regurgitation  of  a 
diminished  volume  of  blood  from  the  aorta,  diminished  in  conse- 
quence of  the  stenosed  mitral  opening.  In  one  case  the  mitral 
lesion  predominates,  and  the  effects  on  the  heart  and  circulation 
are  essentially  the  same  as  in  uncomplicated  mitral  narrowing. 
In  another  this  defect  is  subordinate  to  the  aortic  lesion,  and  the 
secondary  changes  in  the  heart  are  chiefly  such  as  are  found  in 
aortic  insufficiency. 

Symptoms. — The  symptoms  are  consequently  determined  by 
the  predominating  lesion.  In  all  examples  of  this  combination 
there  is  more  or  less  dyspnoea  of  effort,  but  when  the  mitral  sur- 
passes the  aortic  defect  in  gravity  this  symptom  is  more  pro- 
nounced. 

Thus  I  have  observed  two  female  patients  with  this  combina- 
tion. In  one  the  aortic  regurgitation  was  plainly  the  greater,  and 
she  was  able  to  take  a  fair  amount  of  exercise,  even  slow  bicycle- 
riding,  without  special  discomfort.  If  the  effort  became  too  severe 
it  produced  palpitation  and  breathlessness.  The  other  woman  in 
whom  the  mitral  defect  predominated,  and  was  still  further  com- 
plicated by  pericardial  adhesions,  showed  great  hepatic  and  con- 
siderable general  venous  engorgement  and  complained  of  weakness 
and  decided  shortness  of  breath  upon  even  slight  exertion.  Both 
these  patients  broke  down  their  compensation  while  under  my  ob- 
servation, ar.d  in  both  this  rupture  proved  irretrievable.  The  lat- 
ter was  given  a  course  of  baths,  after  having  been  confined  to  bed 
27 


394  DISEASES  OP  THE  HEART 

for  a  number  of  weeks.  They  failed  utterly  to  reinstate  the  heart. 
Digitalis  also  proved  powerless.  Dropsy  did  not  appear,  but  the 
circulation  became  extremely  feeble,  temperature  remained  per- 
sistently subnormal,  falling  on  several  occasions  to  96°  F.,  and 
once  to  95°  F.,  dyspntea  grew  greater,  and  death  took  place  one 
week  after  she  returned  to  her  Dakota  home,  under  what  final 
appearances  I  have  not  been  able  to  learn. 

The  other  patient  considered  herself  in  usual  health  until  mid- 
summer of  1901.  Then,  apparently  as  a  result  of  the  intense  heat, 
the  fatigue  of  a  short  journey,  and  an  attack  of  indigestion,  follow- 
ing a  too  hearty  supper  that  same  day,  she  began  to  suffer  from 
most  annoying  palpitation  whenever  she  walked  .about,  no  matter 
how  slowly.  Weakness  also  set  in,  and  with  the  palpitation  in- 
creased in  spite  of  digitalis  and  other  therapeutic  measures. 
These  symptoms  at  length  obliged  her  to  keep  her  bed,  and  even 
then  her  condition  grew  so  much  worse  that  she  was  brought  back 
to  Chicago. 

I  found  her  in  a  deplorable  plight.  The  pulse  was  extremely 
small  and  weak,  about  100,  and  the  right  appreciably  smaller  than 
the  left.  The  right  arm  and  a  portion  of  the  right  thoracic  wall 
were  cedematous,  in  consequence  of  thrombosis  of  the  external 
jugular,  subclavian,  and  axillary  veins.  The  liver  was  palpable 
and  hard,  but  there  was  no  dropsy  of  the  ankles.  The  bases  of 
the  lungs  were  dull  with  fine  crackling  rales,  and  she  coughed  up 
bloody  sputum.  The  right  heart  was  much  dilated,  and  the  sounds 
and  murmurs  were  feeble.  She  complained  much  of  exhaustion, 
slept  pooi'ly,  and  passed  a  scanty  amount  of  urine  containing  a 
trace  of  albumin. 

After  a  time  dropsy  of  the  legs  set  in,  and  towards  the  close  of 
her  illness  thrombosis  took  place  in  the  veins  of  the  left  side  of  the 
neck,  with  resulting  a'dema  of  the  corresponding  arm.  There  was 
nothing  to  indicate  acute  endocai'ditis,  and  licnce  the  thrombosis 
was  ])robably  due  to  coagulation  of  the  blood  from  pressure  and 
stasis.  This  very  interesting  phenomenon — i,  e.,  venous  throm- 
bosis in  cases  of  heart-disease — has  been  considered  more  fully 
under  Syiii])toms  of  Chronic  Endocarditis  (]).  205). 

Diagnosis. — The  diagnosis  of  combined  mitral  stenosis  and 
aortic  regurgitation  is  made  by  the  discovery  of  the  physical  signs 
of  both  lesions  modified  and  more  or  less  obscured  by  each  other. 


COMBINED   yALVULAR   L?]SIONS  395 

Ins'pection  shows  the  apex-beat  displaced  to  the  left  and  down- 
ward, as  in  aortic  incompetence,  but  to  a  less  extent.  If  the  steno- 
sis is  considerable,  and  has  led  to  right-ventricle  hypertrophy, 
there  is  epigastric  pulsation,  and  there  may  also  be  visible  engorge- 
jnent  of  the  superficial  veins. 

On  palpation  the  displaced  apex-beat  is  found  to  be  less  forci- 
ble and  heaving  than  in  pure  aortic  regurgitation,  and  there  is  a 
more  or  less  distinct  and  prolonged  presystolic  thrill,  depending 
on  the  degree  of  mitral  constriction.  The  characters  of  the  pulse 
are  also  found  modified.  By  reason  of  the  stenosis  it  is  small  and 
weak,  while  the  aortic  lesion  gives  it  a  collapsing  character.  In  one 
of  my  patients  mentioned  above  this  was  fairly  well  marked,  while 
in  the  other  it  was  not  appreciable  by  the  finger,  the  pulse  being 
distinguished  by  smallness  and  lowness  of  tension.  In  cases  in 
which  the  mitral  obstruction  is  the  dominant  lesion  palpation  is 
also  likely  to  detect  more  or  less  hepatic  enlargement. 

Percussion  discovers  increased  cardiac  dulness  in  all  diame- 
ters, and  is  of  great  aid  in  the  determination  of  the  coexistence 
of  these  two  lesions.  Mitral  stenosis  does  not  cause  increase 
of  dulness  to  the  left  of  the  nipple ;  and,  conversely,  aortic 
regurgitation  does  not  occasion  increase  of  dulness  to  the  right. 
Yet  in  this  combined  lesion  dulness  is  increased  in  both  these 
directions.  Consequently,  the  results  of  percussion  taken  in 
connection  with  those  of  auscultation  are  of  the  greatest  possible 
importance. 

Auscultation. — This  also  furnishes  valuable  information,  al- 
though it  should  never  be  relied  upon  to  the  exclusion  of  the  sec- 
ondary physical  signs  perceived  by  the  other  means  of  investiga- 
tion. The  mitral  disease  is  shown  by  a  characteristic  presystolic 
murmur  at  the  apex  and  by  accentuation  of  the  pulmonic  second 
sound,  the  aortic  insufficiency  by  a  diastolic  bruit  in  the  aortic 
area  or  upon  the  sternum,  and  transmitted  downward  and  to  the 
left,  while  the  secoild  tone  in  the  second  right  interspace  is  enfee- 
bled or  absent.  If  in  doubt  concerning  the  significance  of  this 
murmur,  one  should  auscultate  the  femoral  artery,  since  when 
aortic  regurgitation  is  also  present  there  is  a  sharp  systolic  snap, 
and  it  may  be  also  a  double  murmur  in  this  vessel.  Extreme 
mitral  stenosis  in  its  late  stages  may  occasion  pulmonary  incom- 
petence with  a  diastolic  bruit,  and  therefore  auscultation  of  the 


396  DISEASES  OF  THE   HEART 

feniorals  is  of  greatest  importance  in  the  differentiation  of  this 
iusnfficiencv  from  aortic  regnrgitation. 

Prognosis. — -The  prognosis  depends  iqxtn  the  degree  of  the 
two  lesions  and  u})on  which  predominates ;  yet,  on  the  whole,  the 
conrse  is  likely  to  be  that  of  mitral  stenosis. 

MITRAL    REGURGITATION    AND    AORTIC    STENOSIS 

A  moment's  reflection  wdll  convince  one  of  the  exceeding 
seriousness  of  this  combination.  The  obstruction  to  the  outflow 
into  the  aorta  serves  to  intensify  the  regurgitation  into  the  auri- 
cle, because  the  blood  flows  in  the  direction  of  least  resistance, 
which  in  this  case  is  backward  rather  than  forward.  If  the  steno- 
sis is  extreme,  it  leads  to  great  stasis  and  exerts  all  the  local  and 
constitutional  effects  of  a  most  pronounced  regurgitation.  The 
heart  becomes  enlarged  in  its  entirety,  but  the  hypertrophy  of  the 
left  ventricle,  instead  of  overcoming  the  obstruction,  serves  but  to 
intensify  the  force  of  regurgitation.  The  work  of  maintaining 
the  circulation  falls  chiefly  on  the  right  ventricle,  and  as  this  is  a 
thin-walled  chamber,  capable  of  but  limited  compensatory  hyper- 
tro])hy,  it  will  not  long  be  able  to  keep  up  the  unequal  struggle. 

Symptoms  are  those  of  mitral  disease  of  an  extreme  degree, 
and  do  not  need  to  be  recapitulated. 

Diagnosis. — The  pulse  is  small  and  feeble,  while  its  rate  and 
rhythm  are  determined  by  the  state  of  compensation.  The  apex- 
beat  is  displaced  downward  and  outward,  and  relative  cardiac 
dulness  is  increased  in  all  directions.  Two  systolic  murmurs  are 
audible,  one  in  the  mitral  area,  and  one  in  the  aortic,  which  are 
to  be  distinguished  from  each  other  by  their  different  points  of 
maximum  intensity,  by  their  propagation,  and  by  their  different 
quality.  The  former,  blowing  and  softer,  is  transmitted  to  the 
left,  while  the  aortic,  lower  pitched  and  rougher,  is  propagated 
upward  into  the  arteries  of  the  neck.  There  is  intensification  of 
the  pulmonic  second  and  diminution  of  the  aortic  second  sound. 
The  chief  difficulty  of  diagnosis  does  not  lie  in  recognising  the 
presence  of  the  mitral  insufhciency,  but  in  determining  whether 
or  not  this  is  relative,  in  consequence  of  dilatation  of  the  left  ven- 
tricle scfoTidary  to  the  long  existing  aortic  stenosis. 

Prognosis. — Under  the  most  favourable  circumstances  the 
prognosis  is  grave,  since  the  compensation  on  the  part  of  the  right 


COMBINED   VALVULAR   LESIONS  307 

ventricle  is  likely  to  be  short  lived,  and  when  once  ruptnred  can- 
not possibly  be  restored.  jMoreover,  both  pulmonary  and  tricuspid 
insufficiency  are  likely  to  result  when  compensation  fails,  and  then 
render  the  prognosis  hopeless, 

AORTIC    REGURGITATION    AND    MITRAL 
REGURGITATION 

This  combination  is  not  infrequently  encountered  in  the  late 
stages  of  aortic  insufficiency  when  dilatation  of  the  ventricle  has 
led  to  relative  incompetence  of  the  auriculo-ventricular  valve.  It 
may,  however,  be  seen  as  a  combined  lesion  when  both  defects  are 
the  result  of  structural  alteration.  The  combination  is  a  grave  one, 
and  yet,  as  stated  by  Bacelli,  a  double  regurgitation  of  the  kind 
under  discussion  does  not  begin  to  be  so  serious  as  obstruction  at 
the  aortic  and  leakage  at  the  mitral  ostium. 

Symptoms. — The  influence  of  the  mitral  lesion  is  to  lessen 
the  effect  of  the  aortic  regurgitation  on  the  general  system,  since 
a  part  of  the  blood  intended  for  the  aorta  is  diverted  into  the  auri- 
cle, and  the  arterial  system  is  not  so  violently  distended  by  each 
blood-wave.  Arterial  tension  does  not  present  such  a  striking  con- 
trast during  systole  and  diastole  as  in  uncomplicated  insufficiency 
of  the  semilunar  valve.  Tor  this  very  reason,  however,  the  arte- 
rial blood-supply  to  the  various  organs  and  tissues  is  diminished, 
and  there  is  marked  arterial  ansemia. 

In  addition  there  are  the  symptoms  of  venous  congestion,  only 
limited  by  such  capacity  for  compensatory  hypertrophy  as  resides 
in  the  right  ventricle.  The  heart  is  likely  to  attain  enormous  size, 
as  shown  by  the  position  of  the  apex-beat  far  to  the  left  of  the 
nipple  and  downward,  and  by  great  increase  of  both  relative  and 
absolute  cardiac  dulness. 

Diagnosis. — This  is  not  usually  a  matter  of  much  difficulty. 
The  pulse  is  small  yet  collapsing,  and  there  is  increased  dulness 
both  to  left  and  right.  Auscultation  reveals  both  a  basic  diastolic 
and  apex  systolic  bruit,  with  feebleness  of  the  aortic  second  ac- 
centuation of  the  pulmonic  second,  and  often  absence  of  the  sys- 
tolic sound  at  the  apex.  Inspection  and  palpation  disclose  passive 
congestion  of  the  venous  system  and  abdominal  viscera.  In  ease 
the  diastolic  bruit  is  likely  to  be  thought  a  mitral  diastolic  one, 


398  DISEASES  OF  THE   HEART 

its  real  nature  may  be  ascertained  l)_v  auscultation  of  the  femoral 
arteries. 

Prognosis. — When  the  combined  defects  are  both  primary,  a 
fair  degree  of  compensation  may  bo  attained  and  preserved  for  a 
time.  When,  however,  cardiac  adequacy  is  once  seriously  im- 
paired, there  is  but  small  prospect  of  its  restoration.  If  the  mitral 
leak  is  secondary,  it  indicates  such  a  grave  loss  of  ventricular  tone 
as  to  make  practically  h()i)eless  the  possibility  of  again  closing 
up  the  mitral  orifice  by  treatment,  no  matter  how  skilful  and  ener- 
getic it  may  be.  This  was  shown  by  the  history  of  the  cases  nar- 
rated in  the  cluipter  on  Aortic  Regurgitation. 

AORTIC    STENOSIS    AND    AORTIC    REGURGITATION 

This  combination  is  not  very  infrequent,  but  does  not  exist  so 
often  as  the  diagnosis  is  made.  This  holds  true  particularly  with 
regard  to  cases  of  aortic  incompetence.  The  rough  systolic  mur- 
mur so  commonly  heard  in  persons  who  present  unequivocal  signs 
of  free  regurgitation  through  the  aortic  ostium  leads  most  inex- 
perienced auscultators  to  conclude  that  there  must  also  be  stenosis. 
This  inference  is  erroneous,  however,  as  shown  by  necro])sies. 
Vegetations  about  the  orifice,  the  ragged  and  stiff  leaflets,  athero- 
matous patches  on  tlie  surface  of  the  aortic  intima,  are  all  capable 
of  throwing  the  blood-stream  into  audible  vibrations  as  it  passes 
through  the  ring  without  in  the  least  acting  as  an  obstruction,  an 
important  fact  in  its  bearing  on  the  clinical  features  of  the  case. 

In  predominating  aortic  stenosis,  on  the  other  hand,  some  de- 
gree of  regurgitation  is  very  likely  to  occur,  as  has  been  stated  in 
the  chapter  dealing  with  obstruction  at  this  orifice.  The  thicken- 
ing and  rigidity  of  the  valve  flaps,  wliich  ])revent  their  being 
thrown  widely  open  by  the  emerging  stream,  also  intcn-fere  with 
their  complete  closure  as  ventricular  contraction  ends.  T Fence  a 
])(»rtion  of  the  blood-wave  finds  its  way  l)ack  into  the  ventricle.  In 
other  cases  one  of  the  cusps  may  be  fenestrated,  or  for  some  other 
reason  incompetent,  Avhereas  its  fellows  are  not,  being  only  incapa- 
ble of  opening  in  a  normal  manner. 

Symptoms. — The  -symptoms  produced  by  combined  aortic 
stenosis  and  regurgitation  partake  in  cliaracter  and  gravity  of  the 
features  which  are  special  to  the  predominating  lesion.  If  incom- 
petence is  the  greater,  compensation  is  possible  for  years  without 


COMBINED  .VALVULAR  LESIONS  399 

the  individual  being  made  aware  of  its  presence.  If  stenosis  pre- 
dominates and  is  pronounced,  the  left  ventricle  is  not  likely  to 
establish  such  a  degree  of  hypertrophy  as  will  maintain  complete 
adequacy  for  very  long.  The  reflux,  even  if  slight,  as  measured 
by  actual  quantity,  is  yet  sufficient  to  cause  more  or  less  dilatation 
of  the  chamber,  and  hence  the  driving  force  of  its  wall  is  impaired. 
Consequently,  the  patient  is  more  apt  to  notice  some  breathlessness 
and  perhaps  palpitation  under  conditions  that  ought  not  to  affect 
him  were  either  stenosis  alone  or  regurgitation  alone  the  lesion. 

Physical  Signs. — The  physical  signs  are  modified  also  by  this 
combination,  and  display  in  varying  proportion  the  characters  of 
each  defect.  Thus  the  pulse  is  neither  so  large  and  collapsing  as 
in  pure  aortic  regurgitation,  nor  so  small  and  slow  as  in  uncompli- 
cated stenosis,  but  is  collapsing  and  also  small.  Capillary  pulsa- 
tion and  Duroziez's  double  femoral  bruit  are  either  absent  or  very 
imperfectly  obtained. 

The  impulse  of  the  heart  against  the  chest-wall  is  not  so  forci- 
ble and  extensive  as  in  free  regurgitation,  and  the  apex-beat  in  size 
and  displacement  partakes  rather  of  the  character  of  stenosis. 
Hypertrophy  of  the  left  ventricle  is  more  apparent  than  is  its  dila- 
tation, with  thickening. 

The  hand  is  very  apt  to  perceive  a  systolic  thrill  in  the  aortic 
area,  and  percussion  demonstrates  that  the  heart  is  not  so  large  as 
in  uncombined  aortic  insufficiency. 

There  are  two  murmurs,  of  which  the  systolic  is  likely  to  be 
intense  and  rasping,  wdiile  the  diastolic  is  of  inferior  prominence 
in  all  respects.  The  sounds  normally  heard  in  the  second  right 
interspace  and  in  the  cervical  arteries  are  likely  to  be  absent  and 
replaced  by  murmurs. 

Diagnosis. — The  diagnosis  of  this  combination  is  as  a  matter 
of  fact  very  difficult,  and  it  is  often  impossible  to  determine  defi- 
nitely whether  both  conditions  are  united  or  not.  This  is  emphat- 
ically true  if  the  case  is  seen  for  the  first  time  after  compensation 
has  failed.  Relative  mitral  insufficiency  or  pronounced  feeble- 
ness of  the  left  ventricle  may  then  modify  the  pulse,  sounds,  and 
murmurs  in  the  manner  just  described.  However,  if  the  fem- 
oral artery  is  auscultated,  and  the  left  side  of  the  heart  is  accu- 
rately outlined  by  percussion,  Duroziez's  sign  will  declare  the 
freedom  of  the  reflux,  and  percussion  will  demonstrate  the  enor- 


400  DISEASES  OP  THE  HEART 

mous  enlargement  of  the  left  ventricle  secondary  to  free  regurgita- 
tion without  obstruction. 

A  moderately  slow,  small,  yet  collapsing  pulse,  a  vigorous, 
rather  circumscribed,  not  greatly  displaced  apex-impulse,  a  systolic 
aortic  thrill  and  bruit  without  powerfulh'  throbbing  and  thrilling 
cervical  arteries,  absence  of  double  femoral  souffle,  and  no  de- 
monstrable capillary  pulse — these  signs,  together  with  a  regurgi- 
tant murmur,  would  justify  the  conclusion  that  stenosis  and  insuffi- 
ciency coexist,  but  that  the  former  probably  predominates.  The 
sphygmograph  ought  to  show  the  rounded  summit  and  anacrotic 
notch  of  obstruction  and  the  ill-sustained  down  stroke  of  regurgi- 
tation (see  Figs.  54  and  66). 

Prognosis. — The  prognosis  of  this  double  defect  is  certainly 
far  from  favourable,  either  as  to  length  of  life  or  as  to  restora- 
tion of  heart-power,  when  this  has  once  given  way.  This  certainly 
applies  to  ju'onounced  stenosis  with  regurgitation,  whereas  it  is 
conceivable  that  a  minor  degree  of  narrowing  might,  by  rendering 
regurgitation  less  free,  serve  to  protect  the  wall  of  the  left  ventricle 
against  the  speedily  damaging  effects  of  free  reflux  through  a 
widely  patent  orifice. 


CHAPTER    XV 

THE    PROGNOSIS    OF    VALVULAR    HEART-DISEASE 
IN    GENERAL 

Something  has  been  said  already  on  the  subject  of  prognosis 
in  the  chapters  devoted  to  the  individual  valve-lesions,  and  there- 
fore some  repetition  will  be  unavoidable.  In  attempting  to  fore- 
cast the  course  and  termination  of  a  given  case  one  should  con- 
sider (1)  the  special  characters  of  the  lesion,  (2)  the  degree  of  the 
secondary  effects  in  the  heart  and  other  organs,  and  (3)  extraneous 
factors  of  age,  temperament,  environment,  etc. 

The  characters  of  valvular  disease  which  influence  prognosis 
are  its  nature,  location,  and  degree,  and  these  cannot  always  be 
considered  separately.  As  a  general  proposition,  it  may  be  stated 
that  stenosis  is  a  more  serious  defect  than  is  regurgitation,  and  yet 
its  gravity  depends  largely  on  its  location.  Furthermore,  the 
amount  of  disturbance  to  the  circulation  is  determined  so  much 
by  the  degree  of  the  local  defect  that  this  latter  may  render  most 
serious  a  valvular  disease,  which  from  its  nature  and  situation 
alone  would  ordinarily  furnish  a  more  favourable  prognosis.  In 
fact  the  forecast  is  so  largely  based  on  the  conditions  of  each  case 
that  one  would  go  far  astray  if  he  were  to  be  guided  by  general 
principles  alone. 

Although  aortic  insufficiency  is  to  be  ranked  first  as  regards 
gravity,  still  a  distinction  should  be  made  between  cases  originat- 
ing in  the  young  in  endocarditis,  commonly  rheumatic,  and  those 
of  atheromatous  origin,  observed  at  or  beyond  middle  age.  In  the 
former  group  great  compensatory  hypertrophy  and  a  healthy 
heart-muscle  may  enable  the  organ  to  functionate  adequately  for 
many  years,  far  longer  indeed  than  do  many  cases  of  mitral  dis- 
ease, although  in  itself  this  latter  is  considered  a  less  serious 
lesion.  On  the  other  hand,  when  aortic  incompetence  is  due  to  a 
sclerotic  process,  the  myocardium  is  rarely  healthy  and  compensa- 

401 


402  DISEASES  OF  THE  HEART 

tion  is  short  lived,  or  indeed  is  never  perfect.  In  snch  a  case  prog- 
nosis is  grave  from  the  start.  It  is  in  this  particular  lesion  that 
sudden  and  unexpected  death  is  likely  to  take  place.  Indeed,  it  is 
almost  the  only  valvular  disease  which  so  terminates,  since  when 
death  occurs  unexpectedly  in  other  defects  it  is  very  exceptionally 
instantaneous,  and  then  is  the  result  of  some  accident,  such  as  em- 
bolism, or  it  terminates  weary  weeks  or  months  of  failing  heart- 
power. 

In  aortic  regurgitation  it  is  not  very  rare  for  patients  to  fall 
dead  unexpectedly  in  the  midst  of  apparently  good  health.  When- 
ever compensation  shows  unmistakable  signs  of  failure,  sudden 
death  in  this  disease  is  not  a  very  remote  possibility.  Moreover, 
compensation  may  be  broken  at  any  time  by  a  rheumatic  attack, 
and  once  impaired  it  is  rarely  restored.  Absence  of  the  aortic 
second  sound  and  dilatation  of  the  left  ventricle  are  therefore 
prognostically  grave,  since  they  indicate  free  reflux  and  feeble 
ventricular  resistance. 

Stenosis  of  the  aortic  ring  presents  a  less  grave  prognosis  than 
does  regurgitation  at  this  orifice.  The  reason  for  this  difference 
is  to  be  found  in  the  effect  of  the  two  lesions  on  the  wall  of  the  left 
ventricle.  A  narrowing  of  the  outlet  leads  to  hypertrophy  with 
relatively  little  dilatation,  unless  of  course  the  obstruction  be  so 
pronounced  that  the  chamber  is  unable  to  empty  itself  during  sys- 
tole, and  stasis  results  behind  the  point  of  constriction.  So  long 
as  the  hypertrophied  ventricle  is  able  to  discharge  its  contents  with 
each  contraction,  and  the  effect  of  the  lesion  is  limited  to  the  ven- 
tricular wall,  the  prospect  of  a  continuance  of  life  for  many  years 
without  distressing  symptoms,  and  even  of  death  at  the  end  through 
some  intercurrent  affection,  is  good.  When,  however,  compensa- 
tion in  this  disease  is  once  destroyed,  there  is  small  likelihood  of 
its  repair,  and  the  prognosis  becomes  very  serious.  Yet  in  this,  as 
other  lesions,  it  is  its  severity,  even  more  than  its  nature  and  loca- 
tion, which  determines  the  degree  of  its  seriousness.  An  extreme 
stenosis  as  regards  length  of  life  is  even  worse  than  free  regurgi- 
tation. When  the  two  lesions  are  combined  the  prognosis  is  as  a 
rule  more  unfavourable. 

Of  the  two  mitral  defects,  it  is  generally  conceded  that  stenosis 
is  the  more  serious.  One  reason  for  this  is  that  the  disease  is  not 
stationary,  but  tends  to  grow  more  pronounced  in  consequence  of 


PROGNOSIS  OF  VALVULAR*  HEART -DISEASE  IN  GENERAL     403 

contraction  of  the  newly  formed  fibrous  tissue  and  of  the  increase 
of  fibrine  deposited  upon  the  vegetations.  ^  Another  reason,  as  we 
shall  see  later  on,  lies  in  the  greater  intensity  of  the  secondary 
effects  on  the  heart.  Mitral  regurgitation,  on  the  other  hand,  is 
under  ordinary  circumstances  the  most  favourable  of  the  four 
lesions  situated  in  the  left  heart.  When  the  leak  is  not  too  free  and 
there  are  no  serious  complications,  such  as  aortic  stenosis  and  ad- 
herent pericardium,  the  defect  in  question  is  not  incompatible  with 
long  life  and  great  mental  and  bodily  vigour.  It  is  possible,  how- 
ever, for  the  regurgitation  to  be  so  free  that  this  relatively  benign 
disease  is  thereby  converted  into  a  very  serious  one,  Leyden  states 
that  sudden  death  occurs  in  only  2  per  cent  of  mitral  disease. 

With  the  exception  of  relative  tricuspid  in^ifficiency,  diseases 
of  valves  of  the  right  heart  are  so  infrequent  that  nothing  needs  to 
be  added  to  what  has  been  said  already  concerning  their  prognosis 
in  the  respective  chapters.  Incompetence  of  the  right  auriculo-ven- 
tricular  valves  secondary  to  other  diseases  is  generally  regarded  as 
of  serious  import,  not  because  it  threatens  life  directly,  having,  as 
it  is  said,  a  safety-valve  action,  but  because  it  indicates  serious  dis- 
proportion between  the  degree  of  the  primary  disease  and  the 
strength  of  the  right  ventricle.  If  it  occurs  with  anything  like  the 
frequency  claimed  for  it  by  Gibson,  then  one  should  not  attach 
to  it  a  very  unfavourable  prognosis.  ]S[evertheless  the  degree  of 
importance  to  be  attributed  to  it  depends  much  on  the  nature  of 
the  primary  affection.  If  it  be  secondary  to  vesicular  emphysema 
or  to  valvular  disease  of  the  left  side  of  the  heart,  as  pronounced 
mitral  stenosis,  the  development  of  tricuspid  regurgitation  must 
be  looked  upon  as  an  omen  of  impending  disaster.  This  form  of 
tricuspid  disease  cannot  be  regarded  as  a  separate  and  independ- 
ent affection,  and  therefore  should  be  classed  among  the  secondary 
effects  of  valvular  disease,  which  are  now  to  be  discussed  in  their 
bearing  on  prognosis. 

From  the  foregoing  it  is  evident  that  although  the  nature 
and  seat  of  valvular  defects  influence  their  prognosis,  yet  it  is 
their  intensity  to  which  we  must  chiefly  look  when  directing  our 
attention  to  the  heart.  It  has  been  distinctly  stated  in  previous 
chapters  that  in  estimating  the  extent  of  a  valvular  defect  one 
must  not  rely  upon  the  intensity  of  the  murmur,  but  upon  the  evi- 
dences of  disordered  circulation.     These  are  the  secondary  effects 


404  DISEASES  OF  THE  HEART 

or  signs  which  are  of  such  vahie  oftentimes  in  making  a  diagnosis 
as  Avell  as  in  stating  the  prognosis. 

One  reason  for  the  grave  outlook  in  cases  of  mitral  stenosis 
is  the  fact  that  this  defect  occasions  widespread  stasis  in  the  ves- 
sels of  the  pulmonary  and  venous  systems,  while  the  diminished 
supply  of  blood  to  the  left  ventricle  leads  to  shrinkage  in  the  size 
of  this  cavity.  If  the  left  auriculo-ventricular  opening  has  become 
greatly  reduced  in  diameter,  no  amount  of  vigour  of  the  left  auri- 
cle and  right  ventricle  can  maintain  the  equilibrium  of  the  blood- 
stream. It  is  only  a  matter  of  time  when  the  pulmonary  system 
and  right  heart,  systemic  veins,  and  abdominal  organs  are  bound 
to  become  engorged. 

In  mitral  incompetence,  on  the  other  hand,  the  left  auricle  and 
pulmonary  veins  may  be  able  to  bear  the  brunt  of  the  regurgitat- 
ing stream  for  a  long  time.  Moreover,  the  left  ventricle  undergoes 
hypertrophy,  and  forcibly  ejects  into  the  aorta  all  that  portion  of 
the  blood  that  does  not  escape  into  the  auricle.  There  is  not  so 
marked  a  tendency  to  disturbance  of  general  nutrition.  Yet,  of 
two  typical  cases  of  mitral  disease,  the  one  constrictive  and  the  other 
regurgitant,  if  the  former  with  its  natural  tendency  to  greater  stasis 
actually  displays  less  pronounced  secondary  effects,  it  offers  a 
better  rather  than  a  graver  prognosis,  because  compensation  is 
complete.  The  general  venous  stasis  in  the  regurgitant  case 
evinces  either  such  a  freedom  of  reflux  that  the  parts  behind 
could  not  long  withstand  it,  and  compensation  was  necessarily 
lost,  or  that  compensation  was  not  able  to  take  place  at  all.  Even 
if  treatment  should  succeed  in  reinstating  the  circulation,  still  the 
fact  of  compensation  having  once  been  lost  would  render  the  prog- 
nosis worse  than  it  would  be  in  the  case  of  stenosis  in  which  com- 
pensation had  never  been  impaired. 

Again,  comi)are  a  case  of  perfectly  compensated  insufficiency 
of  the  aortic  valves  with  one  of  extreme  narrowing  of  that  orifice 
in  which  dilatation  of  the  left  ventricle  is  beginning  to  outbalance 
the  hypertrophy,  and  signs  of  stasis  are  appearing  in  the  pulmo- 
nary and  general  venous  systems.  In  one,  secondary  effects  are 
limited  to  the  licart  and  shown  l)y  tlic  ad  jusfiiu'iit  of  the  left  ven- 
tricle to  the  altered  conditions.  In  the  other  they  have  jiassed 
beyond  the  heart  and  invaded  the  remainder  of  the  circulatory 
apparatus.     It  is  ]jlain  tliat  here  the  degree  of  the  lesion  has  re- 


PROGNOSIS  OF  VALVULAR  JIEART-DISEASE  IN  GENERAL     405 

versed  the  usual  order  of  things  as  respects  the  prognosis  in  these 
two  valvuhir  defects. 

The  foregoing  remarks  show  how  unreliable  would  be  a  prog- 
nosis in  valvular  heart-disease,  which  was  not  based  on  a  careful 
study  of  the  extent,  even  more  than  the  nature  and  location,  of  the 
particular  defect,  and  that  individual  cardiac  conditions  deter- 
mine the  relative  gravity  of  each  case.  jSTevertheless,  I  must  re- 
peat that  my  experience  leads  me  to  agree  with  Broadbent  in  the 
opinion  that,  generally  speaking,  aortic  regurgitation  is  the  most 
serious  and  mitral  regurgitation  the  most  favourable  of  the  four 
valvular  diseases  of  the  left  heart.  The  two  stenoses  occupy  an 
intermediate  position,  and  of  these,  mitral  constriction  is  the 
graver.  This  subject  is  still  further  complicated  by  the  consid- 
eration that  there  are  still  other  factors  that  must  be  reckoned 
with.  For  the  most  part  these  are  of  minor  importance,  and 
yet  some  of  them  make  strongly  for  or  against  an  encouraging 
forecast. 

Complications. — The  gravity  of  any  valvular  defect  is  neces- 
sarily enhanced  by  the  existence  of  complications,  although  to 
what  extent  is  determined  in  great  measure  by  the  nature  of  the 
complication.  Intercurrent  acute  disorders,  which  act  as  compli- 
cations while  they  last,  are  considered  by  themselves.  Here  are 
discussed  only  such  chronic  local  alterations  and  diseases  of  other 
viscera  as  must  of  a  necessity  unfavourably  affect  the  course  of 
valvular  lesions.  Pericardial  adhesions,  whether  strictly  internal 
or  such  as  bind  the  heart  to  some  of  the  surrounding  parts,  cer- 
tainly exercise  a  malign  influence,  since  they  interfere  more  or  less 
seriously  either  with  the  establishment  or  the  maintenance  of  ade- 
quate compensation.  Their  effect  is  specially  detrimental  if  by 
fixation  of  a  chamber  in  the  state  of  dilatation  they  prevent  its 
reduction  and  efficient  hypertrophy.  I  have  seen  this  more  than 
once  exhibited  in  a  case  of  mitral  incompetence  in  which  fixation 
of  the  left  heart  threw  extra  strain  upon  the  right  ventricle,  as 
evinced  by  its  ready  dilatability.  When  a  chronic  adhesive  medi- 
astinitis  holds  the  right  heart  adherent  back-pressure  on  the  two 
cav?e  and  liver  is  increased.  The  pseudo-cirrhosis  of  the  liver 
leads  in  time  to  obstinate  ascites,  and  patients  succumb  to  the 
hepatic  complication  long  before  they  would  be  likely  to  die  from 
cardiac  inadequacy  alone.     Moreover,  an  adherent  pericardium 


•106  DISEASES  OP  THE  HEART 

nut  infrequently  renders  futile  therapeutic  efforts  which  prove 
highly  efficacious  in  cases  without  such  complication. 

The  association  of  two  or  more  valve-lesions  affects  prognosis, 
not  by  shortening  life  necessarily,  although  such  is  likely  to  be  the 
effect,  but  by  rendering  impossible  the  development  of  perfect 
compensation  and  compelling  extraordinary  carefulness,  lest  what 
small  measure  of  compensation  already  exists  be  broken  down  alto- 
gether. The  reader  will  find  more  on  this  subject  in  the  chapter 
on  Combined  Valvular  Lesions, 

It  goes  without  saying  that  chronic  nephritis  is  a  very  grave 
complication,  Not  only  does  the  renal  act  badly  on  the  cardiac 
affection,  but  this  latter,  by  lowering  blood-pressure  in  the  renal 
arteries,  intensities  the  insufficiency  of  the  kidneys.  The  evils  of 
uraemia  are  then  likely  to  be  added  to  those  of  defective  circula- 
tion. The  chronic  nephritis  renders  it  unlikely  that  the  patient 
will  live  out  the  term  of  years  that  would  naturally  be  granted  him 
by  his  valvular  defect  alone.  The  kidney  complication  also  ren- 
ders less  availing  all  attempts  to  remove  dropsy  whenever  it 
appears. 

Pulmonary  tuberculosis  is  not  often  seen  in  combination  with 
valvular  disease,  excepting  of  course  pulmonary  stenosis.  When  it 
occurs,  however,  I  believe  it  enhances  the  gravity  of  prognosis,  for 
I  cannot  see  how  they  can  fail  to  react  injuriously  on  each  other. 
Anything  which,  like  valvular  disease,  impairs  nutrition  must  nec- 
essarily lessen  the  likelihood  of  successful  resistance  to  tubercu- 
losis, while  the  destruction  of  hmg-tissue  must  seriously  affect  the 
already  damaged  heart. 

Harmful  blood-states,  as  chlorosis  and  anoemia,  affect  progno- 
sis in  proportion  to  their  severity  and  their  amenability  to  treat- 
ment. 

Rheumatic  Diathesis — Some  individuals  display  a  marked 
tendency  to  rheinuatic  attacks,  either  acute  or  subacute,  and  every 
now  and  then  suffer  from  pains  in  shoulder,  wrist,  or  other  joints. 
In  such  the  outlook  is  not  bright,  for  the  reason  that  any  one  or  all 
of  these  mild  attacks  may  be  attended  by  fresh  endocardial  inflam- 
mation either  of  the  same  or  other  valves,  or  that  pericarditis  may 
develop.  Even  if  an  active  endocarditis  is  not  excited,  the  changes 
already  set  up  in  the  valves  may  be  rendered  progressive.  Conse- 
quently, a  case  furnishing  favourable  prognosis  originally  may  be 


PROGNOSIS   OP   VALVULAR   HEART-DISEASE   IN   GENERAL     407 

converted  into  one  of  a  most  serious  nature.  In  a  word,  therefore, 
recurrences  of  rheuniatisiii,  n(^  matter  how  mihl,  are  to  be  regarded 
as  affording  a  glo<»my  prognosis  in  any  case  of  valvular  disease. 

Digestive  and  Bronchial  Disorders. — These,  like  rheumatism, 
yet  in  a  different  way,  are  capable  of  unfavourably  affecting  prog- 
nosis. Disturbance  of  the  digestive  function  is  not  infrequently 
observed  in  victims  of  valvular  disease  in  whom  careful  examina- 
tion fails  to  detect  signs  of  secondary  effects  in  other  organs.  The 
chylopoietic  viscera  may  have  their  function  impaired  by  lack  of 
arterial  blood  of  good  quality,  cardiopaths  being  often  anaemic,  or 
in  aortic  cases  by  a  defective  flushing  with  arterial  blood,  or  in 
mitral  patients  by  passive  congestion,  this  last  being  too  slight 
to  be  recognised  by  ordinary  means  of  examination.  Whether  the 
indigestion  is  owing  to  such  causes  or  is  the  result  of  improper 
food  or  faulty  habits  in  eating,  it  is  likely  to  impair  general,  and 
hence  cardiac  nutrition,  and  thus  render  prognosis  less  encour- 
aging. 

A  tendency  to  acute  bronchial  catarrhs  in  mitral  patients  not 
only  evinces  greater  pulmonary  congestion  than  is  otherwise  appar- 
ent, but  also  renders  them  liable  to  an  attack  of  bronchitis,  which 
may  at  any  time  severely  strain  compensation.  In  them,  there- 
fore, prognosis  cannot  be  looked  upon  as  so  favourable  as  if  they 
were  less  sensitive  to  atmospheric  changes  and  did  not  so  easily 
get  up  a  cough,  for  the  severe  expiratory  effort  of  coughing  sub- 
jects the  right  ventricle  to  added  strain. 

Age. — The  prognosis  of  valvular  disease  is  more  serious  at 
either  extreme  of  life  and  most  favourable  in  young  adults.  In 
elderly  individuals  the  myocardium  is  apt  to  be  more  or  less  degen- 
erated, and  although,  as  Leyden  believes,  compensation  is  often 
as  perfect  as  in  the  young,  it  is  more  easily  destroyed.  Further- 
more, the  sclerotic  process,  which  is  usually  responsible  for  the 
valvular  defect,  is  progressive,  and  one  possesses  no  means  of  fore- 
casting whether  these  changes  will  progress  slowly  or  rapidly.  I 
recall  the  instance  of  a  gentleman  of  sixty- four  in  whom  I  detected 
signs  of  aortic  sclerosis  and  probable  coronary  sclerosis  in  explana- 
tion of  his  attacks  of  angina  without  any  evidence  of  valvular  in- 
competence or  of  stenosis.  Yet  at  his  death,  less  than  three  years 
subsequently,  the  autopsy  disclosed,  I  have  been  informed,  well- 
marked  insufficiency  of  the  atheromatous  aortic  valves,  signs  of 


408  DISEASES  OF  THE  HEART 

the  lesion  having  developed  and  been  detected  by  his  physician 
some  months  prior  to  his  death. 

The  gravity  of  the  prognosis  in  childhood  is  attributable  to  a 
variety  of  canses.  In  the  first  place,  the  heart-muscle,  although 
free  from  degenerations,  is  easily  exhausted.  The  chest  is  small 
and  affords  scant  room  for  the  often  enormous  hearts  observed  in 
children  with  long-standing  valvular  disease.  Any  one  who  has 
seen  much  of  valvular  disease  in  children  must  have  observed  that 
they  are  strikingly  unconscious  of  symptoms  which  in  adults  occa- 
sion complaint.  They  are  highly  sensitive  to  pain,  yet  appear  to 
pay  no  attention  to  palpitation  and  shortness  of  breath  during 
play ;  although  the  onlooker  may  observe  tumultuoTis  action  of 
the  heart,  hurried  breathing,  and  cyanosis.  Children  are  therefore 
very  likely  to  overstrain  their  already  damaged  hearts ;  and  that 
this  does  not  occur  more  frequently  is  quite  remarkable.  These 
little  ones  are  excitable  and  emotional,  and  therefore  unable  to 
exert  the  self-control  so  often  necessary  for  the  preservation  of 
compensation.  They  often  display  astonishingly  vigorous  appe- 
tites and  overload  their  stomachs  with  the  sweetmeats  and  dainties 
they  crave,  and  are  permitted  by  indulgent  parents  to  have.  These 
ferment  with  the  formation  of  gas,  which,  distending  the  digestive 
organs,  causes  them  to  crowd  upward  upon  and  still  further  em- 
barrass the  heart  in  its  action.  Lastly,  rheumatism  in  childhood 
is  so  insidious  and  atypical  that  it  is  very  frequently  overlooked. 
Prompt  and  efficient  treatment  is  not  instituted,  and  this  disease 
being  frequent  in  early  years  of  life  excites  fresh  attacks  of  endo- 
carditis, lights  up  a  pericarditis,  or  renders  existing  valve-lesions 
progressive.  Mitral  stenosis  in  young  children  is  particularly  un- 
favourable. It  may  be  briefly  stated  that  valvular  disease  at  this 
period  of  life  is  very  likely  to  end  fatally  before  the  patient 
reaches  adult  age  either  directly  or  tlirough  complications. 

Temperament. — This  possesses  a  not  unimportant  relation  to 
the  prognosis  of  the  diseases  now  under  consideration.  The  pa- 
tient who  is  impulsive,  impetuous,  and  thoughtless  is  like  a  child 
unaccustomed  to  self-control,  and  if  required  to  exercise  self-re- 
straint frets  and  chafes  in  spirit.  Such  a  person  will  be  forever 
committing  indiscreet  acts,  and  will  only  acquire  with  difficulty 
that  patience  and  equipoise  of  spirit  whicli  serve  as  ballast  to 
damaged  hearts.      Individuals  given  to   outbursts  of   anger,   to 


PROGNOSIS   OF   VALVULAR  HEART-DISEASE   IN  GENERAL     409 

worry,  to  fretting  over  trifles,  and  who  appear  never  to  become 
reconciled  to  their  physical  disability,  can  never  be  expected  to 
retain  their  compensation  so  avcII  or  so  long  as  will  those  who 
always  have  themselves  well  in  hand.  Verily,  all  cardiopaths 
should  bear  in  mind  that  Bible  utterance,  "  He  that  ruleth  his  own 
spirit  is  greater  than  he  that  taketh  a  city." 

Sex. — Mitral  disease,  and  in  particular  mitral  stenosis,  is  more 
frequent  in  the  fair  sex,  while  men  are  more  subject  to  aortic  in- 
sufficiency. In  a  sense,  therefore,  sex  may  be  said  to  exert  a  gen- 
eral influence  upon  prognosis.  The  inquiry  that  now  concerns  us 
is  how  does  sex  affect  the  prognosis  of  a  given  valvular  lesion  after 
it  has  once  been  established,  without  reference  to  its  nature.  In 
other  words,  what  is  the  relative  prognosis,  ceteris  'paribus,  of  the 
same  defect  in  the  two  sexes.  This  is  a  very  difficult  matter  for 
decision,  since  it  involves  questions  of  habits,  occupation,  etc. 
Females  are  exposed  to  certain  perils  of  pregnancy  and  child- 
bearing,  while,  on  the  other  hand,  men  have  to  encounter  even 
greater  dangers  incident  to  occupations  that  often  produce  cardiac 
overstrain.  The  reader  will  find  these  influences  discussed  at  some 
length  in  the  chapter  on  Treatment  of  Valvular  Disease  in  Gen- 
eral. One  respect  wherein  women  usually  furnish  a  more  favour- 
able prognosis  than  do  males  is  that  of  habits — that  is,  a  greater 
freedom  from  the  injurious  efl^ects  of  excess  in  tobacco,  alcohol, 
and  venery.  Women  are  generally  held  to  be  more  emotional  and 
excitable  than  men,  yet  in  the  matter  of  self-control  they  seem  to 
me  to  possess  an  advantage  over  their  brothers.  The  most  marked 
instances  I  have  ever  seen  of  apprehension — nay,  of  alarm  and 
nervous  agitation — lest  the  examination  result  in  the  discovery  of  a 
heart-lesion,  have  been  in  young  men.  The  female  sex  is  more 
prone  to  anaemia  and  chlorosis,  and  the  injurious  influence  of  these 
blood-states  is  too  well  knowm  to  require  more  than  this  passing 
reference.  In  most  other  respects  I  think  the  question  of  sex  re- 
solves itself  into  that  of  the  individual. 

Occupation. — This  exerts  a  powerful  influence  upon  prognosis. 
The  day  labourer  who  earns  his  daily  bread  by  the  sweat  of  his 
brow  cannot  be  expected  to  keep  his  compensation  intact  for  so 
long  as  will  he  whose  vocation  does  not  subject  his  heart  to  the 
possibility  of  overstrain.  All  authors  are  agreed  in  the  declaration 
that  nothing  in  the  daily  life  of  these  patients  affects  their  hearts, 
28 


410  DISEASES  OF  THE   HEART 

and  hence  the  prognosis,  more  disastrously  than  does  severe  and 
prolonged  or  too  oft-repeated  physical  exertion.  This  is  particu- 
larly true  of  mitral  narrowing,  even  in  the  stage  of  compensation. 
Patients  with  well-compensated  insufficiency  of  the  aortic  valves 
may  endure  overstrain  for  a  time  without  apparent  injury ;  but  so 
soon  as  dilatation  of  the  left  ventricle  has  begun  to  gain  the  as- 
cendency over  hypertrophy,  a  continuance  of  the  strain  will  in- 
evitably result  in  a  breakdown,  and  that  too  at  no  very  distant 
date  in  most  instances. 

Habits. — These  are  matters  of  utmost  importance  if  the  lives 
of  patients  with  valvular  disease  are  to  be  prolonged.  They 
should  be  minutely  inquired  into,  therefore,  by  the  medical  at- 
tendant. The  daily  life  of  these  sufferers  should  be  ordered  on 
the  principle  of  moderation  in  all  things.  Whatever  is  injurious 
to  a  healthy  person  is  doubly  so  to  one  wdth  an  unsound  heart. 
Consequently  a  prognosis  which,  as  regards  everything  else,  may 
be  good,  may  be  rendered  very  uncertain,  if  not  actually  bad,  by 
the  discovery  of  evil  practices.  By  these  are  meant  particularly 
excess  in  tobacco,  alcohol,  or  other  narcotics,  and  in  sexual  in- 
dulgence. But  patients  may  also  increase  the  gravity  of  prog- 
nosis by  gluttony,  loss  of  sleep,  exciting  novel  reading,  gaming, 
etc. — in  short,  by  whatever  promotes  nervous  and  cardiac  ex- 
citement. 

Home  Surroundings. — These  include  all  those  n^atters  of  sanita- 
tion, as  dampness,  sunshine,  ventilation,  drainage,  the  ability  to 
obtain  suitable  food  and  clothing,  freedom  or  not  from  domestic 
worry  and  annoyances,  opportiniity  for  recreation,  etc. — in  a  word, 
the  residential  and  social  conditions  which  in  all  of  us  make  for 
happy,  contented  lives. 

The  prognosis  in  the  case  of  the  poor  man  cannot  be  expected 
to  be  as  good  as  that  of  him  w^ho  is  able  to  command  everything 
that  can  minister  to  his  comfort  and  well-being.  If,  e.  g.,  a  pa- 
tient with  mitral  stenosis  or  a  failing  aortic  insufficiency  is  com- 
pelled by  the  exigencies  of  his  purse  or  environment  to  labour  or 
to  ascend  wearisome  flights  of  stairs  or  steep  acclivities  upon  re- 
turning to  his  home,  no  matter  how  often  this  may  be,  he  can 
hardly  be  expected  to  keep  this  up  without  eventually  suffering 
injury.  These  and  many  other  matters  may  seem  too  obvious 
to  require  mention,  and  yet  they  are  details  which  the  physician 


PROGNOSIS  OF   VALVULAR  HEART-DISEASE  IN  GENERAL     411 

must  take  into  consideration  if  he  would,  form  a  reliable  prog- 
nosis. 

The  Probable  Effect  on  the  Patient  of  the  Knowledge  of  his 
Lesion. — This  is  a  matter,  in  my  opinion,  having  a  decided  bearing 
on  prognosis,  and  which,  therefore,  should  be  discussed.  Physi- 
cians and  the  laity  generally  believe  a  cardiopath  must  not  be 
informed  of  the  fact  when  he  is  found  to  have  a  cardiac  defect,  lest 
he  be  alarmed  and  become  morbid  and  introspective.  Doubtless 
there  are  many  nervous,  apprehensive  persons  who  would  be  harm- 
fully affected  by  such  knowledge.  When  such  is  the  case  I  believe 
it  renders  prognosis  less  favourable,  because  if  kept  in  ignorance 
of  his  true  condition  he  is  not  prepared  to  avoid  whatever  may  be 
harmful.  If  detrimental  influences  are  to  be  shunned,  patients 
must  have  explained  to  them  how  and  why  these  are  injurious 
to  them,  since  the  doctor's  dictum  in  this  regard  is  not  enough 
for  an  intelligent  person.  Kept  in  ignorance  or  put  off  with  an 
evasive  answer,  he  may  be  set  to  pondering  and  conjecturing,  and 
hence  to  fancying  his  condition  is  worse  than  it  really  is.  I  be- 
lieve, therefore,  that  it  is  a  positive  gain  to  a  cardiopath  to  acquaint 
him  wath  at  least  a  part  if  not  all  of  the  truth.  Of  course  he  does 
not  need  to  be  informed  with  brutal  abruptness,  but  gently  and  in 
a  manner  calculated  not  to  frighten  him  unduly.  The  individual 
who  cannot  bear  even  a  part  of  the  truth  without  detriment  will 
assuredly  furnish  a  less  favourable  prognosis  than  he  who,  know- 
ing the  truth,  accepts  it  philosophically,  and  determines  to  make 
the  best  of  a  bad  bargain. 

The  Effect  of  Digitalis  on  the  Patient. — It  goes  without  saying 
that  when  valvular  disease  has  reached  such  a  stage  as  to  necessi- 
tate the  administration  of  digitalis  the  prognosis  is  not  good  even 
at  the  best.  Thus  much  any  one  knows,  but  only  a  few,  if  any, 
are  able  to  prognosticate  how  much  longer  the  heart  is  going  to 
bear  up,  even  sustained  by  such  a  prop.  In  such  a  case,  as 
pointed  out  by  Leyden,  a  certain  degree  of  information  may  be 
derived  from  a  study  of  the  effect  of  the  remedy. 

If  the  beneficial  action  of  digitalis  is  quickly  lost  after  its 
administration  has  been  discontinued,  and  the  heart  manifest  its 
need  of  this  tonic  by  a  speedy  return  of  symptoms,  the  prognosis 
is  serious,  for  it  indicates  myocardial  inadequacy.  It  is  a  still 
more  unfavourable  indication  if  from  time  to  time  the  dose  of 


412  DISEASES  OP  THE  HEART 

digitalis  has  to  be  increased  to  maintain  its  effect,  for  it  points  to 
the  not  distant  arrival  of  a  time  when  the  heart  will  cease  to 
respond  to  the  remedy,  and  the  end  will  not  be  far  to  seek. 

The  Relation  of  Prognosis  to  Life  Insurance. — There  was  a  time 
when  an  individual  with  valvular  disease  was  rejected  indiscrimi- 
nately by  all  insurance  companies.  In  England,  and  by  some  com- 
panies now  in  this  country,  some  of  these  patients  are  accepted  as 
"  defective  risks,"'  and  therefore  it  is  in  order  to  discuss  this  sub- 
ject in  this  place.  There  are  two  classes  of  persons  with  valve- 
lesions  whom  I  would  reject  except  possibly  for  a  very  limited 
term  of  years,  and  only  then  at  so  high  a  premium  as  to  make  it 
almost  prohibitive.  These  are  cases  of  pronounced  mitral  steno- 
sis and  insuthciency  of  the  aortic  leaflets.  Even  when  the  latter 
appears  compensated  there  is  always  the  possibility  of  sudden  and 
unexpected  death,  which,  as  already  stated,  renders  prognosis  very 
uncertain.  Stenosis  of  the  left  auriculo-ventricular  orifice  is  pro- 
gressive, and  how  rapidly  this  tendency  will  declare  itself  no  one 
can  foresee.  On  the  contrary,  mitral  regurgitation,  and  to  a  some- 
what less  degree  aortic  stenosis,  may  sometimes  be  considered  rea- 
sonably safe  risks  as  defectives.  It  will  be  noted  that  I  say  some- 
times. This  is  because,  no  matter  how  excellently  the  lesion  may 
be  compensated,  there  are  circumstances  of  individuality  or  en- 
vironment which  determine  prognosis  adversely.  Therefore  the 
examiner  should  consider  exhaustively  and  intelligently  all  those 
factors  which  have  a  bearing  directly  or  remotely  on  the  prospect 
of  the  patient  living  as  long  as  the  characters  of  his  disease  might 
be  expected  to  allow.  Laborious  occupations  and  bad  habits  are,  in 
my  opinion,  a  bar  to  safe  insurance  of  these  risks.  On  the  other 
hand,  a  robust  young  man  who  knows  that  his  mitral  valves  leak, 
and  who  is  determined  to  order  his  daily  conduct  in  a  manner  cal- 
culated to  afford  his  heart  the  very  best  chance  of  carrj'ing  him 
through  to  midille  or  advanced  age,  may  often  ])rove  a  safer  risk 
than  many  another  sound  man  who  banks  on  his  fine  health  and 
splendid  physique. 


CHAPTEE  XVI 

THE  TREATMENT  OF  VALVULAR  HEART-DISEASE 

Feom  a  therapeutic  standpoint,  cases  of  valvular  disease  are  to 
be  divided  into  three  classes,  according  to  the  state  of  compensa- 
tion: (1)  Those  in  which  the  lesion  is  compensated,  (2)  in  which 
compensation  is  incomplete,  and  (3)  in  which  cardiac  inade- 
quacy is  so  pronounced  that  compensation  is  wholly  wanting.  We 
call  a  valvular  defect  compensated  when  the  cardiac  pump,  in 
spite  of  its  defect,  is  able  to  maintain  the  circulation  in  nearly 
or  quite  its  normal  state,  and  there  are  no  symptoms  to  make  the 
patient  aware  of  his  malady.  Under  such  circumstances  laborious 
occuj^ations,  athletic  exercises,  and  games  or  outdoor  sports  re- 
quiring considerable  strength  and  agility  are  endured  without 
more  breathlessness  or  palpitation  than  are  usual  with  persons 
having  sound  hearts.  In  the  second  class,  patients  are  still  able  to 
perform  their  daily  duties  and  engage  in  some  of  the  less  severe 
sports,  but  it  is  with  more  or  less  distress  and  evident  signs  of  heart- 
strain.  There  are  different  degrees  of  imperfect  compensation  in 
this  class,  and  hence  it  is  one  of  wide  limits.  In  the  third  class, 
in  which  compensation  is  wholly  lost,  patients  are  not  only  inca- 
pacitated for  physical  exercise,  but  the  circulatory  disturbance  is 
shown  by  stasis,  generally  by  oedema,  and  by  subjective  symptoms 
that  are  present  even  when  the  patient  is  at  rest.  When  compen- 
sation is  perfect,  examination  of  the  heart  discloses  the  existence 
of  a  lesion,  but  no  secondary  effects  in  the  general  circulation.  In 
the  second  class  signs  of  more  or  less  visceral  and  venous  conges- 
tion are  detected,  although  subjective  symptoms  may  be  insignifi- 
cant, and  in  the  third  these  reach  their  severest  grade.  It  is  evi- 
dent, therefore,  that  treatment  appropriate  to  the  last  stage  is  not 
indicated  in  the  first.  ISTeither  do  patients  whose  compensation  is 
still  maintained  intact  require  the  same  strict  management  as  do 
those  who  are  beginning  to  manifest  failing  heart-power.     Conse- 

413 


414  DISEASES   OP  THE   HEART 

qiieiitlv,  ill  dealing  with  the  inanagemeiit  of  valvular  heart-disease, 
I  shall  consider  it  with  reference  to  the  three  divisions  just  made. 

I.  COMPENSATION  BEING  STILL   PERFECT 

The  object  of  management  in  this  stage  is  the  maintenance  of 
cardiac  power.  Occasionally  a  j)atient  with  valvular  disease  seeks 
medical  advice  for  the  purpose  of  learning  how  he  can  preserve  his 
heart  in  statu  quo.  As  a  rule,  however,  such  a  compensated  lesion 
is  discovered  accidentally  by  the  physician,  wdio  is  then  confronted 
by  the  query  whether  in  case  the  patient  is  ignorant  of  his  heart- 
disease  he  should  be  informed  of  it  or  not.  I  hold  that  in  such  a 
case  the  answer  must  depend  upon  the  circumstances  of  the  case, 
such  as  the  temperament  of  the  individual,  his  habits,  and  the 
nature  of  his  employment  and  manner  of  life.  If  the  knowledge 
that  he  has  heart-disease  is  likely  to  frighten  him  and  render  him 
introspective,  then  the  knowledge  would  better  be  withheld,  unless, 
of  course,  he  is  leading  a  kind  of  existence  calculated  to  break 
down  his  compensation.  Under  such  circumstances  it  may  be  nec- 
essary, and  the  part  of  wisdom,  to  inform  him  that  his  heart  is  not 
sound,  and  is  likely  to  be  damaged  by  his  manner  of  living.  In 
such  an  instance,  however,  the  information  should  be  imparted  in 
a  manner  not  calculated  to  create  needless  alarm.  If  the  individ- 
ual is  reasonable  and  cool-headed,  particularly  if  his  pursuits  are 
active,  I  believe  he  should  be  jilaiiily  told  of  the  existence  of  his 
valvular  defect,  for,  other  things  being  equal,  the  knowledge  by  a 
person  that  he  has  a  locus  rninoris  resistentltv  is  likely  to  make  for 
a  longer  lease  of  life. 

Since,  then,  the  aim  of  management  in  this  stage  is  to  preserve 
compensation,  the  physician  must  concern  himself  with  the  minut- 
est details  of  the  patient's  daily  life.  lie  would  take  a  narrow 
view  of  a  case  indeed  who  contented  himself  with  the  (piestion  of 
medicinal  treatment.  Conipcnsdtcd  valve-defects  require  not 
dr)i(js,  hut  instruction  upon  the  following  points: 

Exercise. — It  may  be  laid  down  as  a  general  pro])osition  suit- 
able to  all  forms  of  compensated  valve-defects  that  when  any  kind 
of  exercis(!  does  not  produce  sym])toms  of  cardiac  strain  it  may  be 
l)ermitt('(l.  Indexed,  as  will  be  seem  later  on,  judicious  exercise 
j)roiii(it('s  conipensatory  hyjx'i'lrophy  in  some  forms  of  valvular  dis- 
ease.    I'here  are  other  lesions,  however,  which  by  their  very  nature 


THE  TREATMENT  OF  VaLVULAR  HEART-DISEASE         415 

are  theoretically  likely  to  and  often  actually  do  suffer  injury  in 
time  from  severe  bodily  exertion.  This  statement  applies  particu- 
larly to  cases  of  mitral  stenosis.  If  the  left  auriculo-ventricular 
opening  is  but  slightly  constricted,  considerable,  even  severe  physi- 
cal effort  may  be  endured  without  symptoms,  but  as  a  rule  some 
shortness  of  breath  is  experienced,  and  patients  should  be  explic- 
itly warned  against  persisting  in  their  exertion  when  dyspnoea  is 
felt.  The  effect  of  muscular  contraction  and  deepened  respiration 
incident  to  exercise  is  acceleration  of  the  flow  of  venous  blood  to 
the  right  heart  and  lungs.  If  the  blood  cannot  readily  pass  the 
mitral  ring,  it  becomes  dammed  back  in  the  left  auricle  and  pul- 
monic veins,  engorging  and  overstraining  the  right  ventricle.  This 
may  resist  the  stress  for  a  time,  but  if  the  strain  is  too  prolonged 
or  too  frequently  repeated  the  cardiac  walls  finally  yield  and  the 
hypertrophy,  upon  which  adequate  compensation  depends,  is  su- 
perseded by  dilatation.  Therefore,  patients  with  pronounced 
mitral  stenosis,  even  when  compensated,  should  be  cautioned 
against  violent,  prolonged,  or  too  oft-repeated  exercise  of  a  severe 
kind.  Hurrying  up  stairs  or  hills,  running,  and  even  very  rapid 
walking,  fast  bicycle-riding,  sports  and  games  that  necessitate  run- 
ning and  springing  without  frequent  pauses  to  permit  recovery  of 
breath — e.  g.,  furious  sparring,  wrestling  and  fencing,  lawn-tennis, 
basketball,  and  the  like — are  among  the  kinds  of  exercise  particu- 
larly likely  to  harm  patients  with  mitral  stenosis,  even  when  com- 
pensated. On  the  other  hand,  if  they  indulge  moderately,  they 
may  enjoy  rowing,  paddling,  and  bowling.  Billiards,  golf,  and 
croquet  are  specially  suited  to  them,  while  some  may  be  permitted 
to  hunt,  and  nearly  all  to  fish.  When  the  constriction  is  not  pro- 
nounced, gentle  horseback  riding,  slow  bicycling,  and  even  the 
lighter  kinds  of  gymnasium  work  are  permissible.  In  specifying 
the  kind  of  exercise  and  sport  to  be  allowed,  the  physician  should 
always  bear  in  mind  the  personal  equation.  The  degree  of  the 
lesion  and  the  gravity  of  its  secondary  effects,  even  more  than  the 
nature  of  the  lesion,  determine  the  patient's  ability  to  endure  exer- 
cise without  harm.  The  individual  temperament,  judgment,  and 
power  of  self-restraint  are  also  of  great  importance.  The  physi- 
cian must  endeavour  to  inform  himself  as  accurately  as  possible 
regarding  the  effect  of  any  given  kind  of  exercise  on  the  particu- 
lar patient  before  coming  to  a  decision. 


416  DISEASES  OF  THE  HEART 

What  lias  been  said  of  mitral  stenosis  applies  also  to  cases  of 
aortic  obstruction  when  this  is  pronounced.  Slight  narrowing  of 
this  orifice  is  often  compatible  with  great  muscular  exertion  and 
active  exercise.  When,  however,  compensation  is  once  broken  in 
these  cases,  it  is  repaired  with  difficulty,  if  indeed  at  all,  and  there- 
fore good  judgment  and  careful  study  of  each  case  are  essential  to 
a  wise  decision.  In  these  cases  exercise  should  not  be  carried  to 
the  production  of  palpitation,  particularly  prolonged  palpitation. 
The  wall  of  the  left  ventricle  is  susceptible  of  far  greater  hyper- 
trophy than  is  that  of  the  right;  besides  the  effect  of  an  aortic 
stenosis  is  confined  for  a  time  at  least  to  the  ventricle,  and  does 
not  embrace  the  thin-walled  auricle,  and  consequently  exercise  is 
likely  to  be  better  endured  than  when  the  obstruction  is  at  the 
mitral  opening. 

The  next  in  order  on  an  ascending  scale,  as  regards  its  ability 
to  withstand  the  effects  of  exercise,  is  mitral  regurgitation.  In 
this  disease,  owing  to  the  circumstance  that  during  diastole  there  is 
no  impediment  to  the  filling  of  the  ventricle,  and  notwithstanding 
that  a  portion  of  the  blood  gushes  back  during  systole  into  the  auri- 
cle, there  is  not  the  same  degree  of  engorgement  in  the  parts  back 
of  the  seat  of  lesion  as  in  mitral  constriction.  Of  course  the  meas- 
ure of  the  heart's  resistance  is  governed  by  the  degree  of  the  incom- 
petence and,  as  in  all  valve-lesions,  by  the  state  of  the  heart-muscle. 
If  the  leak  is  very  free,  compensation  is  not  so  apt  to  be  complete 
as  when  the  regurgitation  is  insignificant.  In  cases  of  well-com- 
pensated insufficiency  of  the  mitral  valve  continued  and  severe 
exercise  may  often  be  indulged  in  without  the  production  of  an- 
noying symptoms.  This  statement  applies  to  the  rheumatic  rather 
than  the  atheromatous  form  of  the  lesion.  I  know  an  attorney 
who,  fifteen  years  ago,  when  a  growing  lad,  had  a  pronounced 
though  perfectly  compensated  mitral  insufficiency,  and  who  played 
lawn-tennis  enthusiastically  without  any  other  discomfort  on  the 
part  of  his  heart  than  the  consciousness  of  rapid,  strong  beating  of 
the  organ.  Despite  frequent  injunctions  to  the  contrary,  he  con- 
tinued to  indulge  in  this  sport  during  several  years,  and  is  now 
reported  to  be  so  well  that  lie  does  not  know  he  has  a  heart.  An- 
other of  my  patients,  a  mercliant  past  thirty,  with  a  mitral  incom- 
petence in  a  state  of  admirable  compensation,  is  much  given  to 
sparring  and  broadsword  practice,  which,  he  declares,  never  gave 


THE  TREATMENT   OP  VALVULAR  HEART-DISEASE         417 

him  any  shortness  of  breath  and  only  a  rapid  heart-action,  that 
subsided  so  soon  as  the  exertion  ceased.  "  Such  instances  are  not 
rare,  and  yet  severe  physical  efforts  are  not  without  danger  to  these 
patients. 

Such  as  are  fond  of  manly  sports  should  be  advised  of  the  pos- 
sibility of  cardiac  overstrain,  and  told  to  desist  when  excessive 
palpitation  or  pronounced  dyspna^a  is  experienced.  They  feel  the 
better  for  a  certain  amount  of  outdoor  exercise,  and  when  young 
and  vigorous  in  other  respects  their  heart-muscle,  like  their  skele- 
tal muscles,  is  likely  to  grow  soft  and  weak  if  debarred  from  ath- 
letic sports  altogether.  Other  things  being  equal,  the  state  of  the 
voluntary  muscles  is  a  fair  index  to  the  condition  of  the  cardiac 
muscle.  Of  two  individuals  with  well-compensated  mitral  leakage, 
one  with  well-knit  muscles  trained  to  exercise,  the  other  unaccus- 
tomed to  outdoor  sports  because  of  sedentary  ^^ursuits,  the  latter 
may  break  down  his  compensation  by  some  effort  which  would  be 
no  more  than  child's  play  to  the  former.  It  is  probable  that  per- 
sons with  mitral  regurgitation  would  be  more  likely  to  suffer 
injury  from  long  running  than  by  games  that  necessitate  intermit- 
tent and  short  spurts  of  speed  or  strength.  Mountain-climbing, 
boat-racing,  and  other  forms  of  contest  or  strength,  which  experi- 
ence has  shown  cause  dilatation  of  healthy  hearts,  will  bring  about 
overstrain  of  diseased  ones  more  readily  and  surely. 

As  a  general  rule  cases  of  aortic  regurgitation  should  be  placed 
at  the  top  of  the  list  as  regards  endurance  of  exercise  without 
injury.  This  statement  does  not  apply  to  persons  who  have  ac- 
quired their  aortic  incompetence  after  the  age  of  forty,  and  there- 
fore probably  as  a  part  or  manifestation  of  a  sclerotic  process  that 
may  have  invaded  the  myocardium  also.  In  such,  even  when  com- 
pensation is  still  maintained,  exercise  should  always  be  moderate. 
The  salvation  of  patients  with  this  lesion  depends  on  hypertrophy 
of  the  left  ventricle.  The  great  Stokes  recognised  this  fact,  and 
accordingly  used  to  recommend  active  physical  exercise  to  patients 
with  this  form  of  valve-disease.  Von  Ziemssen  has  stated  that 
upon  one  occasion,  when  visiting  Stokes  in  Dublin,  the  latter 
directed  his  attention  to  a  man  running  along  the  street  behind  his 
wagon,  and  said  that  he  was  one  of  his  patients  with  aortic  insuffi- 
ciency who  was  carrying  out  this  kind  of  exercise  at  his  (Stokes's) 
advice,  for  the  purpose  of  developing  left  ventricle  hypertrophy. 


418  DISEASES  OF  THE  HEART 

Another  of  Stokes's  patients  with  the  same  lesion  was  a  farmer 
who  was  ahle  to  do  a  day's  ploughing  as  well  as  if  his  heart  were 
sound,  and  in  fact  declared  he  felt  the  better  for  the  exercise. 
This  patient  died  of  acute  pericarditis  soon  after  von  Ziemssen 
learned  the  facts  of  his  case,  and  his  heart  was  given  to  von  Ziems- 
sen, who  declared  it  weighed  several  pounds  and  was  the  most 
marked  example  of  coi'  bovlnum  he  had  ever  seen. 

A  well-compensated  aortic  regurgitation  will  endure  arduous 
physical  labour  and  the  most  energetic  kinds  of  exercise  so  long 
as  the  myocardium  is  healthy.  Therefore  it  is  young  or  compara- 
tively young  patients  whose  aortic-valve  disease  is  of  rheumatic 
origin  who  are  able  to  endure  great  physical  exertion  for  many 
years  without  a  breakdown.  Such  patients  are  far  more  likely  to 
be  unconscious  of  the  existence  of  their  cardiac  mischief  than  are 
the  subjects  of  mitral  disease.  In  the  former  cardiac  stress  is 
manifested  not  so  much  by  dyspnoea  as  by  palpitation,  and  if  their 
valve-defect  dates  from  an  attack  of  rheumatic  endocarditis  in 
childhood,  as  is  often  the  case,  they  have  grown  up  so  accustomed 
to  these  palpitations  that  they  are  apt  to  speak  of  them  as  but  a 
manifestation  of  strong  action  of  the  heart.  While  such  patients 
can  be  quite  safely  permitted  considerable  latitude  in  the  matter 
of  exercise,  they  should  nevertheless  be  closely  watched  for  the 
first  evidence  of  failing  compensation.  For  so  soon  as  the  heart 
begins  to  waver  in  its  work,  bounds  must  be  set  to  their  activity. 

Whatever  is  the  nature  of  the  valvular  disease,  the  physician 
should  always  remember  that  after  the  fourth  decade  of  life  arte- 
rial degeneration  is  frequent,  and  the  myocardium  is  likely  to  have 
suffered  changes  depending  thereon.  Consequently,  liberty  in  ex- 
ercise is  more  hazardous  after  than  before  this  period  of  life,  even 
in  the  case  of  old-standing  lesions  that  have  not  previously  inter- 
fered with  active  habits.  From  this  time  onward  increasing  cau- 
tion must  be  observed,  and  heed  given  to  what  may  appear  to  be 
but  trivial  symptoms  of  heart-strain.  Should  a  valve  become  de- 
fective at  this  period  of  life,  either  as  a  result  of  endocarditis  or 
atheroma,  severe  exercise  and  incautious  efforts  of  all  sorts  are 
to  be  forbidden,  even  though  good  compensation  seems  to  have  been 
established.  Every  physician  of  ex]M>rience  is  aware  of  the  readi- 
ness with  which  compensation  fails  after  middle  age.  Fortunately 
for  such  persons  they  have  arrived  at  years  of  discretion,  and  find 


THE  TREATMENT  OP   VALVULAR  HEART-DISEASE         419 

less  difficulty  in  restraining  their  impulses  to  overdo  than  ig  the 
case  with  the  young.  Exercise  must  now  be  had  by  walking,  driv- 
ing, easy  riding,  billiards,  and  golf.  Pulley  weights,  the  Whitley 
exerciser,  clubs,  dumb-bells,  etc.,  if  permitted  at  all,  are  to  be  used 
under  the  supervision  of  the  medical  attendant  or  of  a  nurse  capa- 
ble of  detecting  signs  of  danger.  Moderation  in  all  things  must 
now  be  the  motto  of  these  patients. 

Occupation. — The  principles  underlying  the  matter  of  exercise 
should  also  determine  the  selection  of  a  suitable  occupation  or  the 
decision  whether  or  not  the  patient's  vocation  is  to  be  continued. 
The  following  employments  are  suitable  for  persons  with  mitral 
stenosis :  Book-keeping,  stenography,  banking  in  any  capacity,  or 
other  forms  of  desk-work,  telegraphy,  clerking,  engraving,  watch- 
making, tailoring,  shoemaking,  harness-making,  saddlery,  etc.^ 
and  for  females  the  various  kinds  of  needlework,  typewriting, 
stenography,  and  desk-w^ork.  Employments  that  necessitate  heavy 
lifting  and  the  carrying  of  heavy  parcels,  as  porterage^  running 
up  and  down  stairs,  swinging  of  heavy  hammers,  etc.,  are  injuri- 
ous, since  they  put  added  strain  on  the  right  ventricle.  Dusty 
occupations  induce  catarrhs  and  coughs,  and  in  this  respect  favour 
bronchial  congestion,  to  which  mitral  patients  are  predisposed 
already.  For  the  same  reason  they  should  not  follow  occupations 
which  expose  them  to  vicissitudes  of  weather  and  sudden  changes 
of  temperature.  Of  the  professions,  journalism,  dentistry,  archi- 
tecture, designing,  and  the  various  branches  of  art  work,  are  all 
suitable — while  theology,  law,  and  such  other  vocations  as  require 
public  speaking  put  a  strain  on  the  right  heart  and  are  less  eligi- 
ble. Teaching  is  not  so  bad,  whereas  the  profession  of  medicine, 
especially  a  general  practice,  is  too  arduous  and  involves  too  much 
exposure  for  persons  with  pronounced  although  compensated 
mitral  narrowing.  A  specialty  permitting  office  practice  is  not  so 
objectionable,  and  yet  any  one  with  this  lesion  should  be  discour- 
aged from  studying  medicine,  or  becoming  a  trained  nurse  or  mas- 
seur. 

Work  with  light  tools,  as  carpentering,  joinery,  house-paint- 
ing and  decorating,  and  even  light  gardening,  may  answer  for  some 
cases  of  aortic  disease,  when  not  admissible  for  severe  mitral  ste- 
nosis. Most  of  the  occupations  followed  by  females  are  not  too 
severe  for  mitral  patients  who  have  good  compensation,  excepting 


420  DISEASES  OP  THE  HEART 

such  work  as  requires  the  carrying  of  trays  heavily  loaded  with 
dishes  and  the  frequent  running  upstairs.  A  general  classification 
or  division  of  occupations  may  he  made  as  follows.  Those  that  are 
indoors  and  require  the  use  of  the  mental  faculties  rather  than 
the  muscles  are  suitable  to  mitral  patients  and  persons  with  serious 
aortic  lesions.  Outdoor  employments  and  work  performed  by  the 
muscles  rather  than  the  brain  may  be  endured  by  subjects  with 
compensated  aortic  regurgitation  and  the  slighter  forms  of  aortic 
stenosis  and  some  cases  of  mitral  insufficiency.  Finally,  vocations 
attended  with  much  excitement  or  nerve-strain,  as  locomotive  driv- 
ing, operating  on  the  stock-exchange,  detective  and  police  work 
(these  last  two  for  other  reasons  as  well),  sea-faring,  and  soldier- 
ing, are  unsuited  to  any  form  of  valve-disease,  no  matter  how  excel- 
lent the  compensation.  The  medical  attendant  can  do  much  good 
by  directing  the  choice  of  occupations  for  the  young,  and  in  the  case 
of  those  who  have  developed  disease  after  their  work  in  life  has 
been  fixed  by  pointing  out  how  the  evils  of  the  occupation  may  be 
minimized. 

Habits. — It  has  already  been  stated  that  moderation  should 
be  the  governing  principle  in  the  lives  of  cardiac  patients.  Excess 
of  every  kind,  particularly  in  sexual  indulgence,  is  to  them  most 
injurious.  It  not  only  occasions  a  harmful  degree  of  cardiac  ex- 
citement, but  it  saps  the  strength  and  lowers  the  tone  of  the  nerv- 
ous system.  The  medical  attendant  who  has  charge  of  a  young 
man  with  valvular  disease  neglects  his  duty  if  he  does  not  instruct 
his  patient  concerning  the  evils  of  sexual  excess.  I  have  known 
young  married  people  of  both  sexes  have  their  compensation  seri- 
ously threatened  after  a  few  months  of  unbridled  license  in  this 
regard.  Although  males  are  the  chief  sufferers  in  this  respect, 
women  with  valve-lesions  are  often  made  to  suffer  through  the 
inconsiderate  demands  of  their  husbands. 

The  tobacco  habit  has  l)ocome  so  well-nigh  universal,  and 
youths  are  so  often  addictcnl  to  cigarette-smoking,  that  a  few 
words  regarding  this  habit  are  also  indispensable.  Young  men 
who  are  just  learning  the  seductive  pleasures  of  tobacco  should 
be  strenuously  urged  not  to  form  the  ha])it,  while  those  cardiac 
patients  who  are  already  addicted  to  smoking  should  be  advised 
to  discontinue  it,  or  if  unwilling  to  do  that,  to  keep  the  use  of 
tobacco  well  within  the  limits  of  lianiifiil  excess.     Just  how  many 


THE  TREATMENT   OF, VALVULAR   IIEART-DISEASE  421 

mild  cigars  or  pipcfuls  of  mild  tobacco  a  patient  with  compen- 
sated valvular  disease  may  be  safely  allowed  to  smoke  daily  is  a 
question  impossible  of  general  answer.  The  degree  of  indulgence 
permissible  will  vary  in  different  cases,  and  must  be  determined 
by  careful  observation  of  the  effect  produced  in  each  instance. 
The  inhalation  of  tobacco  smoke  is  most  pernicious,  particularly 
to  individuals  with  mitral  disease,  since  it  will  surely  increase  the 
already  existing  tendency  to  bronchial  irritation.  If  it  be  true 
that  smoking  produces  antemia,  then  those  persons  whose  com- 
pensation depends  upon  adequate  nourishment  of  the  heart-muscle 
cannot  afford  to  have  their  red  blood-cells  impaired.  It  is  well 
known  that  the  unmoderate  use  of  tobacco  occasions  functional 
cardiac  disorders,  and,  according  to  French  authorities,  raises 
arterial  tension.  Since,  then,  a  healthy  heart  may  suffer  from 
tobacco  intoxication,  surely  an  unhealthy  heart  will  experience 
the  ill  effects  even  more  certainly  and  powerfully.  When  tobacco 
deranges  digestion  and  causes  insomnia,  as  it  is  well  known  to  do 
in  some  individuals,  its  use  should  be  peremptorily  forbidden. 
I  have  heard  it  stated,  with  how  much  truth  I  know  not,  that  Sir 
Morell  Mackenzie  was  wont  to  say  that  the  injurious  effect  of 
tobacco  could  be  measured  by  its  influence  upon  salivary  secretion. 
In  other  words,  when  smoking  causes  salivation  and  frequent 
expectoration,  it  is  an  indication  that  the  individual  is  too  suscep- 
tible to  its  influence  to  safely  persist  in  its  use. 

As  regards  the  liquor  habit,  I  do  not  propose  to  enter  into  a 
discussion  concerning  the  food  value  of  alcohol  and  its  effect  on 
the  animal  economy.  Whatever  be  our  views  respecting  the  mod- 
erate use  of  liquor  in  its  various  forms,  we  all  agree  as  to  the 
evils  of  its  excessive  employment.  What  has  been  said  already 
regarding  the  baneful  effect  of  cardiac  excitation  in  cases  of  com- 
pensated valve-lesions  applies  with  added  force  to  the  immoder- 
ate consumption  of  alcohol.  It  goes  without  saying,  that  the  possi- 
bility of  destroying  compensation  is  always  present  when  a  pa- 
tient gives  himself  over  to  a  debauch.  I  am  a  firm  believer  in  the 
medicinal  virtues  of  alcohol,  but  in  the  compensated  stage  of 
valvular  disease  the  heart  requires  no  medicinal  treatment,  and 
the  only  indication  I  can  see  for  an  alcoholic  beverage  is  to  pro- 
mote the  appetite  and  improve  digestion  of  those  individuals  who 
habitually  take  too  little  nourishment  for  the  requirements  of 


422  DISEASES  OF  THE  HEART 

their  damaged  hearts.  The  conclusion  to  which  I  have  arrived, 
and  which  governs  niv  actions  respecting  the  matter  under  dis- 
cussion, is  that  the  young  and  vigorous  with  satisfactory  compen- 
sation do  not  need  alcohol  in  any  form.  Moreover,  the  danger  of 
their  becoming  slaves  to  the  habit  is  so  real  that  the  circumstances 
have  to  be  very  exceptional  which  make  me  incur  the  responsibil- 
ity of  recommending  the  use  of  even  beer  or  wine  to  such  patients. 
If  one  has  been  accustomed  to  a  stimulant  with  his  dinner  then 
I  do  not  interfere  with  his  habit,  contenting  myself  with  a  caution 
against  its  immoderate  use.  The  habit  of  taking  a  hot  toddy 
before  retiring  for  the  night  is  certainly  not  a  good  one,  since,  as 
pointed  out  by  Fothergill,  it  accelerates  cardiac  action,  and 
thereby  robs  the  heart  of  some  of  its  rest  that  ought  to  be  obtained 
through  the  slowing  of  its  contractions  during  sleep. 

Marriage. — The  baneful  effects  of  one  phase  of  married  life 
have  already  been  considered  under  the  head  of  habits.  There 
is  another  aspect  of  the  subject  which  I  propose  to  consider  here. 
For  the  male  who  has  been  warned  against  and  will  avoid  the 
dangers  of  a  too  ardent  love,  marriage  is  certainly  advisable,  since 
it  conduces  to  regularity  of  living,  and  provides  him  with  the 
comforts  of  a  home  that  cannot  be  obtained  in  a  boarding-house 
or  hotel.  In  the  case  of  a  woman  also  it  is  better  to  be  a  happy 
wife  with  a  comfortable  home  and  a  kind,  considerate  husband  to 
minister  to  her  needs  than  to  be  left  alone,  and  possibly  heart 
hungry.  It  is  quite  another  thing  if  she  is  to  become  a  domestic 
drudge,  obliged  to  cook  and  wash  for  the  family  and  to  bear  off- 
spring. It  is  as  regards  the  dangers  of  pregnancy  and  child- 
bearing  for  women  with  valvular  disease,  even  when  compensated, 
that  I  wish  to  discuss  marriage.  Should  a  girl  who  has  a  valve- 
lesion  become  a  wife  ?  is  the  question  often  asked  of  the  medical 
attendant.  It  is  a  most  serious  one  to  answer,  and  puts  an  enor- 
mous responsibility  on  the  medical  adviser.  There  are  many  cases 
of  even  compensated  valvular  defects  in  which  pregnancy  and 
childbirth  are  fraught  with  considerable  risk.  Yet  every  physi- 
cian of  experience  can  prol)ably  recall  numerous  instances  of 
mothers  who  have  successfully  carried  th(Mv  offspring  through  to 
Itirtli,  in  s])ite  of  serious  lieart-disoase.  Let  us  take  up  tlie  valve- 
defects  of  the  left  heart  separatel3\ 

Mitral  disease,  and  of  this  mitral  stenosis  is  the  form  most 


THE  TREATMENT   OP  VALVULAR  HEART-DISEASE         423 

frequently  met  with  in  women.  Theoreticallj^,  this  is  the  lesion 
which  should  be  the  most  seriously  affected  during  the  latter 
months  of  pregnancy  and  the  expulsive  stage  of  labour.  As  the 
gravid  uterus  rises  in  the  abdominal  cavity  and  when  in  the  last 
two  months  its  fundus  interferes  with  the  proper  descent  of  the 
diaphragm,  and  crowds  the  viscera  aside,  dysj^nusa  and  cyanosis 
appear,  and  walking  often  occasions  serious  distress.  The  right 
heart  becomes  embarrassed  in  consequence  of  mechanical  interfer- 
ence with  the  circulation.  The  pregnant  uterus  impedes  the  de- 
scent of  the  diaphragm,  so  that  the  flow  of  blood  out  of  the  great 
veins  and  through  the  right  heart  into  the  lungs  is  deprived  of  the 
aid  resulting  from  full  and  regular  respiration.  Moreover,  the 
pressure  upon  the  intra-abdominal  veins  ^retards  the  return  flow 
from  the  inferior  extremities,  and  blood-pressure  in  the  capillaries 
is  increased.  This  raises  pulse-tension,  and  by  thus  increasing 
peripheral  resistance  throws  greater  work  upon  the  left  ventricle. 
Under  the  most  favourable  conditions  this  chamber  discharges  but 
a  small  volume  of  blood  into  the  arterial  system,  and  when  its  out- 
flow is  still  further  impeded  by  abnormal  peripheral  resistance,  it 
results  in  augmented  stasis  within  the  left  auricle,  pulmonary 
system,  and  right  heart.  The  vicious  circle  already  existing  by 
reason  of  the  mitral  stenosis  and  the  strain  upon  the  right  ven- 
tricle are  intensified.  If  this  is  not  too  severe,  the  woman  may 
be  able  to  endure  her  pregnancy  to  full  term. 

When  at  length  labour  comes  on,  and  the  expulsive  stage  is 
reached,  there  is  imminent  danger  of  the  right  ventricle  giving 
way  under  the  added  stress  of  violent  straining  efforts. 

The  same  condition  obtains  in  mitral  regurgitation,  but  the 
enlargement  of  the  left  ventricle,  which  if  compensation  is  pres- 
ent is  hypertrophied  as  well  as  dilated,  is  a  factor  for  good  by 
enabling  the  heart  to  withstand  increased  peripheral  resistance. 
The  augmentation  of  arterial  tension  would  by  raising  intra- 
cardiac blood-pressure  increase  the  regurgitation  into  the  left  auri- 
cle were  it  not  counteracted  by  the  left-ventricle  hypertrophy. 
The  danger  is  that  the  ventricle  may  not  be  able  to  resist  the 
strain,  in  which  event  the  evils  of  the  mitral  incompetence  become 
intensified,  and  the  right  ventricle  at  length  suffers  from  over- 
strain. Even  if  the  injurious  tendencies  of  pregnancy  are  suc- 
cessfully withstood,  the  woman  with  mitral  regurgitation  is  sub- 


424  DISEASES   OF   THE   HEART 

jected  to  the  same  danger  during  the  second  stage  of  labour  as  is 
one  with  stenosis.  Whether  the  exi)hination  just  given  is  correct 
or  not,  the  danger  to  mitral  patients  during  this  trying  period 
lies  in  pulmonary  engorgement  and  failure  of  the  right  ventricle. 
With  this  peril  kept  constantly  in  mind  the  attentive  accoucheur 
can  often  conduct  the  pregnancy  and  gestation  to  a  successful 
issue. 

Capillary  and  venous  stasis  are  to  be  lessened  by  saline  or 
other  not  drastic  cathartics  and  by  keeping  the  patient  at  rest. 
When  the  expulsive  efforts  of  labour  endanger  the  integrity  of  the 
right  ventricle  or  when  stasis  in  the  lungs  leads  to  pulmonary 
o'dema,  instrumental  delivery  becomes  impel'atively  indicated, 
and  must  not  be  delayed.  In  these  cases  chloroform  is  not  at- 
tended witli  more  than  ordinary  danger. 

In  eases  of  aortic-valve  disease  the  strain  of  childbearing  is 
on  the  left  ventricle.  Regurgitation  through  the  aortic  orifice 
is  likely  to  be  increased,  and  in  aortic  stenosis  the  augmented 
peripheral  resistance  hinders  the  output  from  the  left  ventricle 
in  the  same  manner  as  if  the  orifice  were  for  the  time  being  still 
further  contracted.  Nevertheless,  if  compensatory  hypertrophy 
is  suflicient,  the  left  ventricle  alone,  or  chiefly,  bears  the  brunt  of 
the  struggle.  Tlie  patients  as  a  matter  of  fact  endure  the  ordeal 
of  childbearing  often  without  dangerous  cardiac  embarrassment 
and  better  than  do  mitral  sufferers.  According  to  Davis's  state- 
ments, more  than  50  ])er  cent  of  mitral  and  23  per  cent  of  aortic 
cases  succumb  to  the  dangers  of  pregnancy  and  gestation. 

Only  yesterday  1  saw  a  woman  in  the  seventh  month  of  preg- 
nancy who  prior  thereto  presented  well-marked  evidence  of  mitral 
regurgitation  with  stenosis,  considerable  enlargement  of  the  right 
ventricle,  and  dyspnci'a  of  effort.  Except  upon  walking  for  a 
considerable  distance  and  in  ascending  stairs,  this  patient  yester- 
day evinced  no  ])ron()niiced  signs  of  cardiac  embarrassment,  and 
declared  she  was  not  sjiccially  inconvenienced  by  her  pregnancy. 
Her  pulse  was  only  moderately  accelerated,  appreciably  tense  and 
strong,  and  the  apex-beat  was  powerful,  indicating  adequate 
hypertrophy  of  the  left  ventricle.  There  was  increased  dulness 
to  the  right,  but  it  was  not  excessive,  and  the  right  ventricle  gave 
no  sign  of  being  dangerously  overl)urdened.  If  this  patient  re- 
ceives proper  management  during  the  remaining  two  months,  and 


THE   TREATMENT   OP   VALVULAR  HEART-DISEASE  425 

is  not  permitted  to  overstrain  herself  during  labour,  I  believe  her 
heart  will  not  suffer  damage  from  this,  her  eighth  pregnancy. 
Her  husband,  who  is  a  physician,  states  that  she  had  heart-disease 
at  the  time  of  her  marriage,  fourteen  years  ago. 

The  following  conclusions  may  be  stated:  (1)  Pregnancy  is 
a  condition  of  gravity,  but  not  necessarily  of  peril,  to  women  with 
compensated  valvular  disease.  (2)  Labour  is  a  time  of  real  dan- 
ger, the  extent  of  which  depends  upon  the  nature  of  the  lesion 
and  the  degree  of  compensation,  but  is  often  endured  without 
catastrophe.  (3)  Mitral  disease  is  more  liable  to  disastrous  con- 
sequences from  both  pregnancy  and  gestation  than  are  aortic  de- 
fects. (4)  Even  in  mitral  disease  the  degree  of  danger  depends 
upon  the  state  of  compensation,  (5)  Pregnant  women  with  valv- 
ular disease  require  special  watching  as  labour  approaches,  and 
during  the  expulsive  stage  should  be  delivered  instrumentally  at 
the  earliest  indication  of  dangerous  heart-strain.  (6)  The  perils 
of  marriage  should  be  clearly  stated  to  both  of  the  contracting 
parties,  and  when  compensation  is  imperfect  or  is  maintained 
with  difficulty  they  should  be  advised  not  to  wed.  (7)  Interfer- 
ence with  pregnancy  is  justifiable  only  when  the  nature  and  sever- 
ity of  the  lesion  render  the  maintenance  of  compensation  impossi- 
ble or  when  serious  symptoms  have  already  supervened. 

Clothing. — The  physician  who  would  instruct  his  patient  in 
matters  of  importance  in  maintaining  compensation  must  have 
regard  for  what  sometimes  appear  to  be  things  of  trifling  moment. 
Among  such  details  is  to  be  included  the  clothing.  All  who  have 
much  experience  in  the  management  of  cardiopathies  come  in 
time  to  realize  the  influence  exerted  by  varying  conditions  of 
blood-pressure.  The  reason  of  one  man's  success,  as  contrasted 
with  another's  failure,  in  the  treatment  of  heart-disease  is  often 
found  in  the  close  attention  he  pays  to  undue  rise  of  blood-pres- 
sure. Take,  for  example,  an  ordinary  case  of  mitral  stenosis. 
Without  any  recognisable  change  in  the  cardiac  condition  or  in 
his  daily  conduct,  a  patient  will  be  conscious  that  his  breathing 
becomes  embarrassed  by  efforts  usually  put  forth  without  any 
such  effect.  He  consults  his  medical  adviser,  who,  familiar  with 
the  case,  discovers  by  studying  the  pulse  and  state  of  the  venous 
circulation  that  there  is  unwonted  tension  in  the  arterial  system. 
He  finds,  furthermore,  that  there  is  constipation  perhaps,  and 
29 


426  DISEASES  OP  THE   HEART 

knowing  the  influence  of  this  condition  over  blood-pressure 
through  the  splanchnics,  he  administers  a  mercurial  pill ;  tension 
within  the  abdomen  and  arterial  system  is  lowered,  and  the 
patient's  breathing  returns  to  its  nsual  state.  A  tendency  to  pal- 
pitation in  a  case  of  aortic  regurgitation  may  be  Avholly  due  to 
increased  capillary  resistance  and  be  relieved  by  the  administra- 
tion of  a  vaso-dilator. 

It  is  because  of  the  effect  on  blood-pressure  produced  by  a 
patient's  manner  of  dress  that  the  matter  of  clothing  becomes 
important,  and  may  make  for  or  against  the  establishment  or 
preservation  of  compensation.  Cardiac  sufferers  are  often  very 
sensitive  to  the  cold  and  to  sudden  changes  of  weather,  partly  on 
account  of  a  rheumatic  diathesis  and  partly  because  of  sluggish 
cutaneous  circulation,  as  in  mitral  stenosis,  or  of  relative  arterial 
ana'mia  in  aortic  disease.  Wool  should  therefore  be  worn  next  to 
the  skin,  and  during  seasons  of  low  temperature  the  hands  and 
feet  must  be  kept  warm  by  heavy  not  too  tightly  fitting  gloves 
and  shoes.  It  is  well  to  have  the  latter  constructed  with  cork 
soles,  and  in  very  cold  weather  overshoes  may  be  a  necessity. 
Outer  garments  should  not  only  be  warm,  but  they  must  not  be  so 
heavy  as  to  tire  the  wearer.  It  is  very  important  that  the  clothing 
does  not  constrict  the  vessels.  This  applies  to  shoes,  gloves,  col- 
lars, belts,  and  waistbands  in  the  case  of  males,  and  to  garters, 
corsets,  and  tight  dresses  on  the  part  of  females.  Constriction  of 
the  extremities  tends  to  raise  blood-pressure  as  well  as  to  mechan- 
ically impede  circulation,  and  should  be  corrected  in  every  case  of 
valvular  disease.  Harm  is  chiefly  done,  however,  by  garments 
that  constrict  the  chest  and  abdomen.  A  woollen  undervest  that 
has  become  shrunken  until  uncomfortably  tight,  an  overcoat  that 
is  outgrown,  and  can  be  buttoned  only  w^ith  difficulty,  is  in  a 
measure  at  least  injurious  in  the  same  way  as  is  a  too  tight  corset. 
Xot  only  are  respiratory  movements  hampered  and  venous  circu- 
lation retarded  in  consequence,  but  the  hypertrophied  and  there- 
fore compensated  heart  is  more  or  less  compressed  and  restricted 
in  its  movments;  abdominal  viscera  are  engorged  and  displaced; 
the  play  of  the  diaphragm  is  limited,  and  the  evil  consequences 
of  the  valvular  lesion  itself  are  intensified.  These  effects  are 
evinced  by  increase  of  cyanosis  and  shortness  of  breath,  both  of 
which  disappear  or  lessen  when  the  clothing  has  been  removed. 


THE  TREATMENT  OP  VALVULAR  HEART-DISEASE         427 

Instead,  therefore,  of  suspending  the  skirts  from  the  hips,  to 
effect  which  they  have  to  be  fastened  snugly  about  the  waist,  it 
is  preferable  that  women,  particularly  slender  ones,  wear  gar- 
ments of  one  piece,  so  that  the  weight  may  be  borne  by  the  shoul- 
ders ;  or  they  should  replace  the  ordinary  corset  by  a  corset-waist, 
to  which  the  skirts  can  be  buttoned,  thus  avoiding  constriction  of 
the  waist.  'Not  many  months  ago  I  was  consulted  by  a  lady  on 
account  of  attacks  of  dyspnoea  and  cyanosis,  which  at  times 
amounted  even  to  partial  syncope.  She  presented  signs  of  pro- 
nounced mitral  stenosis  with  considerable  secondary  enlargement 
of  the  heart  and  hepatic  congestion.  She  was  inclined  to  cor- 
pulence, and  to  preserve  her  figaire  wore  a  long,  stiff  corset,  which, 
in  response  to  my  inquiry,  she  declared  was  loose  and  comfortable. 
jSTot  convinced  on  the  poifit,  I  measured  her  waist  both  on  the  bare 
skin  and  outside  of  the  corset,  and  thus  demonstrated  that  when 
her  corset  was  hooked  she  actually  measured  4  inches  less  than 
she  did  next  to  the  skin.  I  then  explained  at  some  length  the 
harm  she  was  doing  herself,  and  succeeded  in  getting  her  to  re- 
form her  mode  of  dressing,  much  to  her  relief,  as  she  subsequently 
acknowledged.  In  this  instance  I  am  convinced  that  the  symp- 
toms of  cardiac  stress  under  conditions  of  exercise  were  due 
largely  to  the  additional  impediment  to  circulation  and  respira- 
tion occasioned  by  the  tightness  of  her  clothing. 

Baths. — I  have  found  in  numerous  instances  that  ladies  with 
valvular  disease  were  in  the  habit  of  taking  a  semiweekly  hot 
bath,  and  some  of  them  confessed  to  lying  in  the  water  for 
twenty  minutes  or  more.  Inquiry  generally  elicited  the  fact  that 
the  bath  was  followed  by  a  feeling  of  languor,  even  amounting  in 
some  instances  to  prostration.  It  is  well  known  that  such  hot 
baths  are  weakening  to  the  heart  and  lower  vascular  tone.  They 
should  be  forbidden  therefore,  and  the  patients  advised  to  content 
themselves  with  a  rapid  sponge-bath  daily  if  strength  permits,  and 
once  a  week  a  tub-bath  of  short  duration,  and  of  a  temperature 
closely  approximating  that  of  the  human  body.  Mitral  patients 
endure  bathing  less  well  than  do  those  with  aortic  lesions.  Yet 
in  all  cases  the  degree  of  latitude  permissible  in  the  matter  of 
baths  is  to  be  determined  by  their  effect.  If  they  are  followed  by 
a  healthy  reaction — that  is,  by  warmth  of  the  skin  and  a  sense  of 
rest  or  well-being — they  are  beneficial;  but  if  a  cardiac  patient 


428  DISEASES  OP  THE  HEART 

finds  his  bath  leaves  him  with  cold  extremities  and  a  feeling  of 
fatigue,  and  that  the  exertion  of  briskly  rubbing  his  body  into  a 
glow  occasions  breathlessness  or  palpitation,  frequent  bathing  is 
likely  to  do  him  harm. 

Swinnning,  whether  in  salt  or  fresh  water,  is  to  be  considered 
not  alone  with  reference  to  the  temperature  of  the  water ;  there 
is  the  shock  of  the  sudden  plunge  or  immersion,  and  also  the 
exertion  of  proi)elling  the  body  while  at  the  same  time  sustaining 
the  weight  or  pressure  of  the  surrounding  liquid.  For  these  vari- 
ous reasons  this  form  of  bathing  is  apt  to  put  a  good  deal  of  strain 
on  the  heart,  and  persons  with  mitral  lesions,  or  those  whose  de- 
fects, of  whatever  nature,  are  maintaining  compensation  with 
difficulty,  should  either  indulge  in  this  sport  not  at  all  or  only 
under  great  restriction,  both  of  frequency  and  duration.  It  is 
probable  that  many  of  the  cases  of  supposed  death  from  cramp  in 
the  water  are  in  reality  instances  of  heart-failure  or  asystolism. 

The  Turkish  and  Russian  baths  and  the  various  modifications 
of  the  shower-bath  or  douche  found  at  health-resorts  affect  the 
heart  and  vascular  system  powerfully,  and  should  not  be  taken 
by  cardiac  sufferers  without  the  advice  of  a  physician  who  is 
familiar  with  their  effects  and  competent  to  decide  on  the  advisa- 
bility of  such  baths  in  each  instance. 

The  saline  and  carbonated  baths  employed  for  therapeutic 
purposes  at  Bad  Xauheim  may  be  left  out  of  consideration  at  this 
time,  since  they  are  not  indicated  for  individuals  whose  valvular 
defects  are  in  the  stage  of  compensation. 

Food. — Of  all  matters  concerning  our  patients  none  is  so  essen- 
tial as  that  of  nourishment,  and  yet  there  is  nothing,  I  venture  to 
say,  about  which  physicians  of  more  than  average  intelligence 
and  experience  are  so  unable  to  give  precise  and  suitable  instruc- 
tions. In  works  on  diet  are. to  be  found  tables  of  various  food- 
stuffs compiled  with  regard  to  the  needs  of  the  human  organism 
under  conditions  of  work  and  repose,  and  from  which  one  may 
construct  dietaries  suitable  to  the  requirements  of  cardiac  patients. 
In  this  chapter  I  shall  only  make  certain  general  statements  that 
apply  to  the  regimen  of  persons  whose  lesions  have  not  greatly 
deranged  circulatory  e(iuii)oise. 

Adequate  compensation  in  any  given  case  implies,  nay,  neces- 
sitates, the  supposition  that  the  circulation  of  the  digestive  appa- 


THE  TREATMENT   0^  VALVULAR  HEART-DISEASE         429 

ratus  is  not  appreciably  disturbed.  The  conclusion  is  warranted, 
therefore,  that  there  is  no  digestive  disorder  secondary  to  the  car- 
diac mischief  and  necessitating  a  corresponding  modification  of 
the  diet.  It  is  only  essential  that  the  food  be  of  good  quality,  well- 
cooked,  and  sufficient.  The  proportion  of  proteids  suitable  to 
each  case  will  be  governed  by  the  amount  of  exercise  taken,  the 
kind  of  work,  and  the  tendency  or  not  to  obesity.  The  same  consid- 
erations apply  to  the  quantity  as  well  as  the  quality.  The  proper 
preparation  of  the  food  is  essential  if  digestive  disorders  are  to  be 
avoided.  It  is  of  importance  also  that  meals  be  taken  at  regular 
hours ;  gluttony  is  injurious,  and  the  amount  of  fluids  taken  with 
meals  should  be  definitely  stated,  10  ounces  being  ordinarily 
sufficient.  Patients  who  are  anaemic  must  be  given  a  liberal  allow- 
ance of  beef,  eggs,  milk,  and  such  vegetables  and  fruits  as  are 
rich  in  iron-forming  compounds;  those  who  incline  to  constipa- 
tion are  to  get  a  dietary  calculated  to  correct  the  tendency.  Tea 
and  coffee  in  moderation  may  be  allowed.  In  a  word,  so  long  as 
compensation  is  complete  there  is  no  indication  for  special  rules 
to  govern  the  dietary  further  than  what  would  be  required  for 
the  preservation  of  health  in  the  same  individual  were  he  not 
afflicted  with  an  incurable  malady. 

Illnesses. — Among  so  many  items  of  importance  in  the  preser- 
vation of  compensation  it  is  difficult  to  specify  one  as  greater  than 
another,  and  perhaps  it  is  not  wise  to  attempt  to  do  so.  Yet  I 
wish  to  lay  particular  emphasis  on  this  point — namely,  no  illness 
or  indisposition,  apparently  trivial  in  itself,  should  ever  be  so 
regarded  in  a  person  who  has  suffered  injury  from  endocarditis. 
This  is  specially  true  of  children.  In  them  rheumatism  is  so  apt 
to  be  masked  that  an  infection  of  the  throat,  a  persistent  pain  in 
an  extremity,  a  rise  of  temperature  without  obvious  cause,  should 
always  receive  careful  medical  attention.  The  intestinal  tract 
affords  so  ready  and  frequent  a  portal  of  infection  that  no  devia- 
tion from  the  standard  of  health  is  to  be  neglected  as  of  no  conse- 
quence. Far  better  is  it  to  bear  the  imputation  of  being  over- 
careful  and  fussy  than  to  some  day  awake  to  the  consciousness 
that  your  neglect  has  permitted  injury  to  visit  one  of  your  pa- 
tients, whose  compensated  valvular  lesion  might  otherwise  have 
gone  on  years  longer.  Tell  your  patients  emphatically  and  clearly 
that  a  tonsillitis,  yes,  or  even  an  acute  eoryza,  is  never  to  be  neg- 


430  DISEASES  OP  THE  HEART 

lected.  Ill  a  case  of  mitral  disease,  particularly  of  stenosis,  an 
attack  of  simple  bronchitis  may  break  down  utterly  the  integrity 
of  the  right  ventricle.  Be  always  suspicious  of  slight  fevers, 
which  to  those  living  in  a  malarial  region  may  appear  to  be  of 
that  nature;  such  a  trivial  yet  persistent  run  of  fever  has  only 
too  often  turned  out  to  be  an  endocarditis.  In  cases  of  pneu- 
monia and  other  serious  affections  cardiac  sufferers  merit  more 
than  ordinary  care  and  watchfulness,  if  they  are  to  come  through 
undamaged.  This  is  particularly  true  of  persons  with  mitral  de- 
fects not  only  because  of  the  possible  lighting  up  of  a  fresh  endo- 
carditis, but  because  the  strain  to  wdiich  the  right  ventricle  is 
subjected  by  reason  of  the  valvular  mischief  is.  enormously  aug- 
mented by  the  pneumonic  consolidation — while  at  the  same  time 
cardiac  endurance  is  impaired  through  the  effect  of  the  pneumonic 
toxines  on  the  myocardium.  If  in  such  a  case  paralysis  of  the 
vaso-motor  centres  leads  to  cyanosis,  the  outlook  is  serious  indeed. 
The  gravity  of  pneumonia,  la  grippe,  and  other  acute  infections, 
gonorrha-a,  diphtheria,  scarlatina,  measles,  puerperal  septica?mia, 
etc.,  in  all  cases  of  compensated  valvular  disease,  is  so  obvious, 
particularly  as  respects  the  liabilit}^  to  fresh  endocarditis,  that 
further  comment  is  unnecessary.  Considerations  of  prophy- 
laxis require,  therefore,  that  our  cardiopaths  be  properly  in- 
structed on  these  points.  If  it  be  objected  that  this  is  likely  to 
render  them  introspective,  and  even  hypochondriac,  or  if  the 
patients  are  children,  then  the  requisite  information  may  be 
imparted  to  the  family,  friends,  or  j)arents.  No  one  need  fear 
that  his  motives  will  be  misunderstood.  Indeed,  I  am  convinced 
that  the  American  public  likes  to  be  talked  to  by  physicians  as  if 
they  were  intelligent  and  reasonable  beings,  and  that  nothing  con- 
duces more  to  the  establishment  of  confidence  in  the  medical  prac- 
titioner than  frankness  and  ])laiii  dealing  in  all  matters  that  con- 
cern the  hcallh  of  his  patients. 

Use  of  Drugs. — It  is  an  error  to  suppose  that  every  individual 
presenting  signs  of  valvular  mischief  requires  medicinal  treat- 
ment. Digitalis  or  some  other  heart-tonic  is  not  to  he  ordered 
in  every  case  in  ivhich  an  endocardial  murmur  is  heard.  Inexpe- 
rienced practitioners  fresh  from  a  medical  college  are  very  apt  to 
commit  this  mistake,  and  consequently  the  foregoing  injunction 
is  not  out  of  ])lace.     When  a  person  willi  valvular  disease  presents 


THE  TREATMENT  OP  VALVULAR  HEART-DISEASE         431 

himself  in  your  office,  inquire  minutely  into  the  matter  of  symp- 
toms, and  if  he  does  not  acknowledge  any  indicative  of  cardiac 
stress,  remedies  influencing  the  heart  directly  are  not  indicated. 
If  you  belong  to  that  class  who  believe  no  person  should  be  allowed 
to  leave  the  physician's  office  without  a  prescription  or  a  drug  of 
some  kind,  lest  forsooth  the  patient  fancy  he  has  not  received  his 
money's  worth,  then  let  it  be  a  placebo.  As  a  matter  of  fact,  there 
are  few  persons  who  cannot  be  satisfied  under  such  circumstances 
with  an  expression  of  opinion  coupled  with  sound  advice  on  the 
points  under  discussion  in  this  chapter.  Careful  inquiry  will 
usually  bring  out  some  pernicious  habit,  faulty  digestion,  consti- 
pation, some  impairment  of  appetite,  etc. ;  or  there  may  be  more 
or  less  anaemia,  bronchial  irritation  perhaps,  monorrhagia,  some 
deviation  from  perfect  health,  which  permitted  to  go  on,  will  in 
time  exert  malign  influence  on  compensation.  Any  such  condition 
calls  for  correction,  and  to  this  end  medicinal  treatment  may  be 
indicated.  What  medicaments  are  suitable  in  each  instance  is,  of 
course,  to  be  left  to  the  judgment  of  the  medical  adviser. 

Although  slight  disturbances  demanding  attention  are  often 
dependent  upon  scarcely  detectable  disorders  of  circulation,  they 
are  not  necessarily  so  in  perfectly  compensated  cases,  and  hence 
these  patients  may  generally  be  treated,  so  far  as  regards  medi- 
cines, as  they  would  be  were  they  wholly  free  from  endocardial 
defects. 

Two  conditions  likely  to  prove  more  injurious  to  individuals 
with  a  valve-lesion,  although  compensated,  than  would  be  the  case 
if  his  valves  had  not  been  damaged,  are  constipation  and  flatulent 
distention  of  the  bowel.  In  both  there  is  splanchnic  irritation 
and  consequent  alteration  of  blood-pressure,  but  in  the  latter  the 
effect  of  mechanical  encroachment  upon  the  contents  of  the  tho- 
racic cavity  must  be  reckoned  with.  Uncorrected  it  may  con- 
tribute materially  to  the  destruction  of  heart  adequacy,  to  say 
nothing  about  the  patient's  discomfort  in  the  way  of  postprandial 
breathlessness  in  mitral  and  tendency  to  palpitation  in  aortic  dis- 
ease. Both  disorders  of  digestive  function  tend  to  impair  the 
appetite,  give  rise  to  neuralgias,  anaemia,  coldness  of  the  extrem- 
ities, and  many  other  phenomena  of  auto-infection.  Moreover, 
flatulent  indigestion,  probably  through  the  absorption  of  toxines, 
is  a  frequent  cause  of  deranged  cardiac  rhythm.     This  not  only 


432  DISEASES  OF  THE  HEART 

annoys  or  even  alarms  the  patient,  bnt  it  may  even  lead  to  the 
development  of  dilatation.  It  is  for  the  relief  of  such  disturbing 
factors  as  these,  therefore,  that  drugs  find  their  legitimate  use  in 
the  management  of  compensated  cardiopathies.  In  most  cases  the 
speediest  and  surest  relief  is  likely  to  be  afforded  by  a  mercurial, 
a  grain  of  calomel  in  divided  doses,  or  5  grains  of  blue  mass,  fol- 
lowed next  morning  by  a  Seidlitz  powder  or  a  glassful  of  some 
laxative  water.  Cascara,  aloes,  rhubarb,  podophyllum,  etc.,  })an- 
creatin,  ox-gall,  nitrohydrochloric  acid,  subgallate  of  bismuth, 
salol  or  salophen,  naphthol  preparations,  etc.,  alone  or  in  various 
combinations  and  with  which  the  reader  is  duly  familiar,  are 
serviceable,  and  will  generally  afford  relief. 

Only  when  gastro-intestinal  disorders  occasion  persistent  de- 
rangement of  cardiac  action  are  digitalis,  strophauthus,  caffeine, 
convallaria,  and  sparteine  to  be  prescribed  in  this  class  of  cases; 
even  then  the  remedy  is  to  be  withdrawn  so  soon  as  the  arrhyth- 
mia or  acceleration  of  the  pulse  has  been  corrected.  Temporary 
palpitation  or  vertigo  on  the  part. of  aortic  patients  nuiy  generally 
be  removed  by  minute  doses  of  glonoiu.  ^wij  ^<^  tttt  '*1'  ^  grain  at 
intervals  of  two,  three,  or  four  hours,  either  alone  or  in  conjunc- 
tion with  3  to  5  drops  of  digitalis.  When  compensation  has  been 
seriously  threatened  by  cardiac  overstrain  or  some  other  disturb- 
ing factor,  digitalis  and  strychnine  may  be  needed  in  addition  to 
rest  and  restricted  diet ;  but  in  all  such  instances  rest  in  bed  for 
a  few  days  is  unquestionably  the  agency  of  greatest  value,  and 
should  be  rigidly  enforced  until  the  period  of  danger  is  past ;  not 
until  then  is  the  patient  to  be  permitted  to  resume  his  usual  mode 
of  life  and  to  return  to  his  wonted  exercise.  In  this  class  of  cases 
"  eternal  vigilance  is  the  price  of  safety." 

Change  of  Climate,  with  Special  Reference  to  High  Altitude. — 
The  question  is  so  often  asked  whether  a  ])aticnt  with  heart-dis- 
ease should  go  to  Colorado  or  make  the  journey  over  the  moun- 
tains to  California,  that  it  seems  best  to  discuss  this  subject  here 
when  foiisidering  those  conditions  llint  make  for  tlic  ])resorvntiou 
of  comjxMisation.  It  is  quite  generally  the  opinion  among  medi- 
cal men  that  the  existence  of  a  valvular  lesion  contra-indicates 
residence  in  elevated  climates.  This  is  too  sweeping,  as  shown  by 
clinical  observation.  My  medical  friends  in  Colorado  assure  me 
that  their  patients  with  valvular  disease,  of  whatever  kind,  suffer 


THE  TREATMENT   OP   VALVULAR   HEART-DISEASE  433 

no  nioro  inconvenience  from  their  heart-lesions  in  Denver  or 
Colorado  Springs  than  do  })ersons  similarly  affected  at  the  sea 
level.  Moreover,  Kegnard,  in  an  elaborate  work  on  the  effect  of 
high  altitude  on  the  heart  and  circulation,  expresses  the  opinion 
that  cardiac  lesions  j^ei-  se  do  not  contra-indicate  residence  in  the 
mountains  when  this  is  necessary,  and  that  aside  from  the  discom- 
fort of  becoming  accustomed  to  the  high  altitude  individuals 
afflicted  with  heart-disease  do  not  experience  permanent  harm. 
^Nevertheless,  he  would  not  advise  residence  in  such  a  climate  for 
a  cardiopath,  since  there  is  nothing  in  his  disease  calling  for  such 
a  climatic  treatment.  This  opinion  impresses  me  as  too  broad, 
judging  from  the  experience  of  some  of  my  cardiac  patients.  I 
have  known  persons  with  mitral  and  aortic  regurgitation  to  visit 
Colorado,  and  there,  at  an  elevation  of  6,000  feet,  to  take  consid- 
erable exercise  without  discomfort,  and  apparently  without  harm. 
Others  with  vascular  and  cardiac  degeneration  have  found  the 
same  to  be  true  with  them,  and  in  fact  one  gentleman  was  actu- 
ally able  to  walk  with  more  ease  at  7,000  feet  than  in  Chicago. 
On  the  other  hand,  my  patients  who  were  not  able  to  endure  high 
altitude  were  sufferers  from  mitral  stenosis,  aortic  stenosis,  and 
mitral  incompetence,  when  complicated  by  pericardial  or  pleu- 
ritic adhesions.  These  cases  were  all  reported  and  discussed  by 
me  in  a  paper  before  the  American  Climatological  Association  in 
1899,  and  will  be  found  in  the  Transactions  of  that  year.  Singu- 
larly enough,  Dr.  Sewall,  of  Denver,  in  discussing  my  paper, 
stated  that  at  that  very  time  he  had  under  observation  in  Denver 
a  female  with  pronounced  mitral  stenosis,  who  had  formerly  been 
under  my  care  in  Chicago,  and  who  was  able  to  endure  the  eleva- 
tion, not  only  of  Denver,  but  also  of  Cripple  Creek  situated  at  an 
altitude  of  about  12,000  feet.  She  died  a  year  subsequently,  I 
understand,  and  I  have  often  wondered  if  her  residence  at  that 
elevation  did  not  aid  materially  in  shortening  her  life. 

As  the  discussion  of  theories  is  foreign  to  the  spirit  of  this 
work,  I  shall  not  discuss  at  length  the  considerations  which  make 
me  conclude  that  residence  in  high  altitudes  is  likely  to  prove 
injurious  to  persons  having  stenosis  or  regurgitant  lesions  com- 
plicated by  pericardial  or  pleural  adhesions.  Suffice  it  to  say 
that  the  effect  of  a  rarefied  atmosphere  is  acceleration  and  small- 
ness  of  the  pulse,  together  with  increase  in  the  depth  and  fre- 


434  DISEASES  OP  THE   HEART 

qiieucj  of  the  respirations,  the  degree  of  this  effect  depending 
of  course  upon  the  degree  of  the  altitude.  The  blood  flows  to 
the  heart  more  rapidly,  and  if  there  is  an  obstruction  at  one  of  the 
orifices,  this  acts  as  a  barrier  to  the  rapid  and  easy  passage  of  the 
blood,  which  tends  to  accumulate  back  of  the  hindrance.  In 
mitral  or  aortic  stenosis  this  would  be  in  the  lungs  and  right  heart, 
and  hence  symptoms  due  to  this  engorgement  are  likely  to  result. 
If  adhesions  exist,  they  interfere  more  or  less  with  the  expansion 
of  the  thorax,  which  takes  place  in  high  climates,  and  consequently 
they  ought  to  hinder  that  adjustment  to  altered  conditions,  which 
is  essential  if  one  is  to  become  accustomed  to  a  high  altitude. 
Further  reflection  and  observation  since  the  publication  of  my 
paper  on  this  subject  have  led  me  to  the  belief-  that  probably  all 
or  nearly  all  individuals  with  valvular  diseases  can  endure  an 
altitude  of  6,000  to  10,000  feet  without  injury,  provided  they  do 
not  take  much  exercise.  Until  they  have  grown  accustomed  to 
the  rarefied  air  they  should  not  walk  at  all,  but  remain  in  bed. 
At  least  such  is  tlie  opinion  and  advice  I  give  when  consulted 
on  this  important  question.  Finally,  it  is  probable  that  much  of 
the  dyspnoea  and  palpitation  complained  of  by  some  at  high  alti- 
tudes is  due  in  part,  perhaps  largely,  to  the  fact  that  in  the  moun- 
tains the  walks  are  not  level.  Hill-climbing  is  trying  for  cardio- 
paths,  even  at  the  sea  level,  and  at  an  elevation  where  the  air  is 
thin  such  an  exertion  could  readily  prove  doubly  injurious.  The 
phenomena  of  mountain-sickness — that  is,  rush  of  blood  to  the 
head,  with  vertigo,  and  even  nausea,  or  in  extreme  cases  bleeding 
from  the  nose  and  ears — are  liable  to  attack  healthy  persons  at 
too  higli  an  altitude,  particularly  during  physical  exertion.  In 
their  milder  degrees  they  may  affect  cardiopaths  in  transit  to  and 
from  the  Pacific  coast,  but  apart  from  these  unpleasant  symptoms 
patients  who  remain  at  rest  in  the  car  need  not  apprehend  serious 
results  even  in  passing  the  loftiest  points.  When  vertigo  or  a 
tendency  to  syncope  is  experienced,  relief  usually  follows  the  ad- 
ministration of  a  diffusible  stimulant  and  the  assumption  of  the 
rccundjcnt  position.  Nevertheless,  caution  would  suggest  the  tak- 
ing of  the  less  lofty  routes. 


CIIAPTEK    XVII 

THE    TREATMENT    OF  VALVULAR    HEART-DISEASE 

(CoriHrmed) 

II.  COMPENSATION  BEING  IMPERFECT 

A  WANT  of  perfect  compensation  may  have  either  one  of  two 
explanations.  It  may  have  never  been  adequately  developed  after 
the  subsidence  of  the  acute  process  that  led  to  the  valvular  mis- 
chief, or  having  been  once  established  it  may  be  destroyed  in  con- 
sequence of  a  variety  of  causes.  In  the  first  instance  the  develop- 
ment of  complete  compensation  may  be  impossible,  owing  to  the 
extent  of  the  damage  sustained  by  the  valves,  in  consequence  of  de- 
generation of  the  myocardium,  or  of  the  coexistence  of  complica- 
tions or  conditions  residing  in  the  patient's  temperament,  environ- 
ment, etc.  In  such  a  case  the  course  of  the  disease  is  generally 
too  short  to  admit  of  its  being  brought  into  the  category  of  chronic 
valvular  affections.  For  the  same  reasons  a  long-continued  main- 
tenance of  compensation  may  be  impossible  after  it  has  once  be- 
come established.  In  many  cases,  however,  it  is  possible  to  arrest 
the  do-wnward  tendency  and  restore  heart-power  when  the  injuri- 
ous influences  are  discovered  and  removed.  If  these  cannot  be 
removed,  then  their  baneful  effects  must  be  counteracted  by  all 
those  therapeutic  measures  which  are  at  our  disposal. 

In  the  management  of  compensated  valvular  disease  the  physi- 
cian conducts  a  defensive  campaign,  so  to  speak,  whereas  when 
compensation  has  failed,  he  is  called  on  to  wage  an  active  offensive 
warfare  against  all  those  forces  that  are  striving  to  destroy  his 
patient.  His  success  depends  not  only  upon  the  skill  with  which 
his  therapeutic  weapons  are  wielded,  but  also  upon  the  precision 
of  his  orders,  and  the  faithfulness  with  which  these  are  executed. 
The  treatment  of  valvular  disease  in  this  stage  requires  also  atten- 
tion to  details  of  daily  life,  no  matter  how  trivial  they  may  appear 
to  be,  and  the  recognition  of  complications.     Moreover,  there  are 

435 


436  DISEASES   OF  THE   HEART 

few  patients  in  whose  envirdiuiicnt  inilucnccs  do  not  exist  which, 
if  permitted  to  i;o  on,  will  not  act  nnfavonrably  and  retard  the 
restoration  of  adecpiate  eonqjensation.  For  this  reason  these  ninst 
be  ascertained  and  removed  so  far  as  is  possible.  It  is  plain, 
therefore,  that  the  proper  management  of  these  cases  consists  in 
mnch  more  than  the  mere  administration  of  heart-tonics  or  other 
medicinal  remedies.  That  highly  gratifying  results  follow  such 
strict  and  careful  management  is  shown  by  the  narration  of  the 
next  three  cases. 

Miss  N.,  referred  by  Dr.  Minor,  of  Asheville,  N.  C,  was  first 
seen  by  me  in  July,  1898.  She  had  spent  the  preceding  winter 
in  Asheville,  and  had  there  sought  medical  advice  in  the  early 
j)art  of  summer  because  of  increasing  difficulty  of  breathing  in 
walking,  the  altitude  being  2,200  feet  and  the  nature  of  the 
ground  hilly.  The  winter  immediately  previous  had  also  been 
passed  in  Asheville,  but  without  her  having  noticed  the  same 
shortness  of  breath.  She  gave  a  history  of  inflammatory  rheu- 
matism three  years  before,  and  a  year  and  a  half  before  of  an  ill- 
ness which,  judging  from  her  account,  must  have  been  an  inflam- 
mation of  a  serous  membrane  within  the  thorax.  Her  age  was 
twenty-two.  Her  pulse  was  much  accelerated,  120  or  more,  regu- 
lar, and  equal.  The  ankles  were  edematous,  and  the  abdomen 
was  distended  by  the  greatly  engorged  liver.  The  broad,  fairly 
powerful  apex-beat  was  found  immovably  fixed  in  the  sixth  inter- 
costal space,  near  the  anterior  axillary  line,  and  superficial  car- 
diac dulness  extended  somewhat  beyond  the  right  sternal  margin, 
upward  to  the  third  costal  cartilage  and  at  the  left,  almost  to  the 
mamillary  line.  There  was  an  intense  blowing  systolic  apex-mur- 
mur transmitted  to  the  left  and  accompanying,  not  replacing,  the 
first  sound,  the  pulmonic  second  sound  being  very  accentuated. 
I  |)(in  auscultation,  fine  crackling  rfdes  were  detected  dui'ing  in- 
spiration along  the  upper  and  left  border  of  prspcordial  dulness, 
and  upon  the  arms  being  raised  and  lowered  a  creaking  sound 
could  be  plainly  heard  at  the  superior  boundary  of  dulness  on  the 
sternum. 

In  tliis  case  it  was  manifestly  not  so  mucli  the  mitral  leak  that 
was  serious,  as  it  was  the  fixation  of  the  left  ventricle  that  was 
preventing  the  maintenance  of  compensation.  Moreover,  it  was 
foreseen   that  diuitalis  aixl   similar   remedies  could   exercise   but 


THE  TREATMENT  OP  VALVULAR  HEART-DISEASE         437 

limited  control  over  the  heart,  since  only  slight  if  any  reduction 
in  the  dilatation  of  the  left  ventricle  was  possible  by  reason  of 
the  restraining  adhesions.  Efforts  had  to  be  directed,  therefore, 
to  lessening  the  resistance  residing  in  the  congested  portal  system 
and  at  strengthening  the  right  ventricle.  The  former  was  to  be 
accomplished  by  purgatives,  tonic  doses  of  digitalis,  and  the  re- 
moval of  all  constricting  clothing ;  the  latter  by  those  same  means, 
re-enforced  by  abstaining  from  too  much  physical  exertion,  and  if 
need  be  by  rest  from  all  exercise.  Accordingly  the  patient  was 
told  to  give  up  her  corset,  which  she  did,  to  take  an  aperient 
water  daily  before  breakfast,  and  thrice  daily  15  drops  of  tincture 
of  digitalis.  Stair-climbing  was  forbidden.  Directions  regarding 
the  quantity  and  kind  of  food  and  the  amount  of  fluids  were 
added.  The  degree  of  improvement  was  so  insignificant  during 
the  next  few  weeks  that  at  length  absolute  rest  in  bed  was  advised 
and  acted  upon.  Then  benefit  became  at  once  apparent  in  slowing 
of  the  pulse  and  diminution  of  dulness  over  the  right  heart.  The 
liver  also  began  to  shrink,  urine  grew  more  abundant,  and  oedema 
disappeared.  After  five  weeks  of  enforced  rest  the  patient  was 
permitted  to  gradually  resume  her  ordinary  mode  of  life,  except- 
ing that  she  was  not  allowed  to  go  out.  All  this  time  digitalis 
or  strophanthus  was  continued  in  about  the  same  dose  (15  drops) 
of  the  one  and  10  drops  of  the  latter  thrice  daily,  with  excep- 
tion of  every  sixth  day,  when  it  was  omitted.  Apex-impulse  grew 
somewhat  stronger,  but  never  altered  its  position  in  the  least ;  the 
marked  change  was  in  the  right  ventricle  and  liver. 

After  a  few  weeks  longer  of  such  management  it  was  decided 
to  try  the  effect  of  a  course  of  ]!Tauheim  baths.  They  were  given 
in  her  home  and  not  at  my  rooms,  as  was  then  the  rule  with  pa- 
tients whom  I  subjected  to  this  treatment.  Whether  because  I 
could  not  watch  their  effect  as  closely  in  this  way,  or  on  account  of 
the  hampering  effect  of  the  adhesions  (I  believe  it  was  the  latter), 
the  baths  did  not  produce  a  beneficial  effect.  Heart-rate  increased 
and  showed  a  tendency  to  unsteadiness,  dulness  to  the  right  be- 
came increased,  and  the  amount  of  urine  diminished.  They 
were  discontinued,  therefore,  and  no  permanent  harm  resulted. 
Considerable  difficulty  was  experienced  in  getting  this  patient  to 
give  up  her  candy  and  obey  instructions  as  to  diet ;  but  the  habit 
of  making  her  furnish  me  with  an  account  of  what  she  ate  and 


438  DISEASES  OF  THE  HEART 

drank  finally  convinced  lier  that  I  was  in  earnest,  and  now  her 
obedience  to  orders  is  all  that  can  be  desired.  In  this  case  men- 
struation is  too  profuse  and  somewhat  irregular;  so  that  she  has 
been  instructed  to  remain  in  bed  during  her  menses,  and  hydras- 
tin  hydrochlorate  is  sometimes  administered.  During  the  summer 
of  1899  her  health  was  quite  satisfactory,  and  she  was  able  to 
enjoy  a  number  of  outings  with  friends  without  very  irksome  re- 
striction on  her  pleasures.  She  has  been  very  subject  to  annoying 
pains  in  her  shoulders,  but  especially  in  her  chest  beneath  the  ster- 
num, and  upon  several  such  occasions  there  has  been  a  circum- 
scribed, faint,  yet  distinct  friction  directly  above  the  superior  line 
of  cardiac  dulness,  which  was  taken  to  indicate  a  fresh  lighting 
up  of  mediastinitis.  These  attacks  have  generally  yielded  to 
counter-irritation  and  antirheumatic  remedies. 

Towards  spring  of  1900  her  condition  began  to  run  down 
slowly  but  surely,  and  complaint  of  "  rheumatic  pains  "  was  fre- 
quent ;  the  pulse  quickened,  and  her  flesh  grew  flabby  and  cold. 
She  consented  to  enter  a  hospital,  where  her  temperature  could 
be  carefully  watched,  as  the  possibility  of  endocarditis  was  enter- 
tained. Temperature  remained  subnormal,  however,  rather  than 
febrile.  Ilcr  urine  was  collected  and  examined,  with  the  follow- 
ing result :  Total  amount  in  twenty-four  hours,  GGO  cubic  centi- 
metres; specific  gravity,  1.028;  urea,  3  per  cent;  2f  per  cent  .of 
albumin ;  numerous  hyaline  and  granular  casts.  Animal  food 
was  withheld,  copious  draughts  of  water  insisted  upon,  and  citrate 
of  potash  was  administered,  together  with  moderate  doses  of  fox- 
glove in  tincture.  A  week  later  the  urine  amounted  to  2,500 
cubic  centimetres,  had  a  specific  gravity  of  1.013,  urea  1.3  per 
cent,  neither  albumin  nor  casts.  This  must  have  been  a  mild 
nephritis  and  not  merely  congestion,  since  the  kidneys  responded 
so  well  to  the  free  intake  of  fluids.  As  was  to  be  expected,  the 
patient's  condition  improved  rapidly,  the  pulse-rate  decreased 
strikingly ;  and  two  weeks  afterward  she  returned  home.  It  is 
now  four  months  later,  and  albumin  has  not  again  been  found  in 
the  urine.  She  has  been  allowed  animal  food  but  sparingly,  and 
has  been  required  to  driidc  wat(n-  freely  between  meals,  with  the 
result  of  her  feeling  iiiiusually  well,  and  being  able  to  enjoy  a 
moderate  amount  of  walking  again,  "^riiis  lady  is  an  invalid,  to 
be  sure,  who  has  to  lead  a  restricted  existence;  but  she  is  able  to 


THE   TREATMENT  OF  VALVULAR   HEART-DISEASE  439 

attend  matinees  and  social  functions  of  a  quiet  kind,  in  fine,  to  get 
a  good  deal  of  enjoyment  out  of  life.  Slic  cannot  entertain  the 
hope  of  becoming  a  wife  and  mother,  and  has  been  so  informed. 

In  this  case  digitalis  has  been  taken  most  of  the  time,  because 
it  has  been  repeatedly  prov'ed  by  trial  that  when  discarded  en- 
tirely its  need  is  shown  after  a  few  days  by  increased  breathless- 
ness  and  subjective  as  well  as  objective  rapidity  of  the  heart's 
action,  to  120  or  more.  The  tincture  has  generally  been  pre- 
scribed, sometimes  10  drops  once  daily,  and  at  other  times  5,  7, 
or  10  drops  two  or  three  times  a  day.  Upon  a  few  occasions 
scantiness  of  the  urine  and  oedema,  shown  by  pitting  of  the 
ankles,  has  necessitated  the  administration  of  the  fresh  infusion 
of  English  leaves,  a  tablespoonful  three  or  four  times  daily.  JSTow 
and  then  citrate  of  potassium  has  been  added.  Sulphate  of  strych- 
nine has  also  been  taken  much  of  the  time,  and  whenever  she  has 
felt  more  than  usual  weakness  she  has  profited  much  from  the 
compound  syrup  of  hypophosphites. 

She  has  been  dependent  on  medicinal  remedies,  but  no  doubt 
a  large  part  of  her  really  good  condition  is  owing  to  the  excellent 
care  she  has  taken  of  herself.  She  has  dressed  sensibly,  wearing 
a  loosely  fitting  corset- waist,-  and  so  far  as  possible  suspending 
her  skirts  from  her  shoulders.  Walking  has  been  done  at  a  slow 
pace  and  for  short  distances,  care  being  taken  not  to  walk  against 
a  strong  wind,  and  to  stop  for  rest  whenever  shortness  of  breath 
or  palpitation  has  been  experienced.  Ascending  stairs  has  been 
avoided,  or  when  that  was  impossible  they  have  been  mounted 
a  few  stairs  at  a  time,  with  frequent  pauses  to  let  her  heart  quiet 
down  or  to  recover  breath.  During  stormy  weather  she  has  either 
remained  indoors  or  has  driven  in  a  closed  carriage  to  her  destina- 
tion. Any  indisposition,  however  trivial,  has  received  prompt 
attention,  and  a  day  of  unwonted  fatigue  or  exertion  has  been 
generally  followed  by  rest  in  bed  or  on  a  couch.  Her  dietary  has 
been  simple  and  nutritious,  and  she  has  not  been  permitted  to  be 
in  the  least  constipated.  On  the  contrary,  she  took  an  aperient 
water  every  morning  for  a  year  at  least,  with  a  dose  of  calomel 
whenever  her  liver  showed  more  than  ordinary  congestion  or  she 
felt  a  sense  of  fulness  about  the  waist.  Latterly  the  laxative 
water  has  been  taken  only  every  other  day.  Finally,  she  has  been 
required  to  see  me  at  regular  intervals,  generally  two  or  three 


440  DISEASES  OF   THE   HEART 

times  a  month,  that  thei'el)y  t^hc  mii;ht  he  kej)t  inuler  control.  In 
her  case  certainly  eternal  vigilance  has  been  the  price  of  safety. 

Master  W.  B.,  aged  eight,  was  examined  by  me  in  June,  1896, 
at  request  of  Dr.  John  Streeter.  He  was  a  frail,  undersized,  pale 
boy,  whose  whole  life  had  been  one  of  many  illnesses ;  broncho- 
pneumonia five  times  in  early  childhood,  innumerable  attacks  of 
fever,  with  coated  tongue,  pain  in  the  right  hypochondrium,  nau- 
sea, and  irritable  stomach,  which  had  generally  yielded  to  calo- 
mel and  milk  diet,  and  had  been  considered  "  storms  of  uric 
acid."  For  a  year  prior  to  my  visit  patient  had  been  under  treat- 
ment by  Dr.  M.  Allen  Starr,  of  New  York,  who,  it  was  stated,  had 
administered  bromide  of  soda  every  night  during  the  year.  The 
mother  had  tirst  learned  of  her  boy's  heart-disease  in  April,  1890. 
Patient  was  very  subject  to  attacks  of  acute  tonsillitis,  having  but 
just  recovered  from  one,  and  at  the  time  of  my  examination  had  an 
acute  coryza.  He  had  the  facial  appearance  indicative  of  adenoids, 
breathed  through  the  mouth,  and  beneath  the  angle  of  the  left 
inferior  maxilla  the  neck  was  tumefied  by  enlarged  cervical 
glands.  His  chest  was  long,  narrow,  sunken  below  the  clavicles, 
prominent  in  the  prtecordium,  and  expanded  poorly  on  inspira- 
tion ;  the  finger-ends  were  noticeably  bulbous,  but  there  was  no 
cyanosis.  The  heart  was  greatly  enlarged,  there  was  a  loud,  harsh 
systolic  apex-murmur  of  wide  propagation,  and  both  liver  and 
spleen  were  palpable  with  much  corroborative  increase  of  dulness. 
The  little  fellow  suffered  from  dyspna'a  and  occasionally  palpi- 
tation on  ascending  stairs  or  hurried  walking.  Urine  was  scanty 
and  of  high  specific  gravity,  otherwise  negative.  His  appetite 
was  capricious,  digestion  weak,  and  bowel  movements  irregular. 

It  w^as  my  opinion  tliat,  if  much  improvement  was  to  be  at- 
tained, three  things  would  have  to  be  done — the  removal  of  the 
nasal  obstruction,  the  development  of  the  chest,  and  the  improve- 
ment of  the  blood  condition.  The  adenoids  could  have  been 
safely  removed  under  ether  and  even  chloroform  skilfully  ad- 
ministered, and  thus  the  first  step  taken  towards  proper  ex})ansion 
of  the  chest.  I  have  notes  of  a  simihir  condition  in  a  boy  of  five 
or  six,  which  was  successfully  oj^erated  on  without  the  slightest 
untoward  effects  as  regarded  his  mitral  insufiiciency  and  with 
ultimate  benefit  to  the  child.  In  \]n\  ])resent  case  the  mother 
wanted  the  treatment  of  the  nasal  obstruction  postj)oned,  and  I 


THE  TREATMENT   OF^  VALVULAR   HEART-DISEASE  441 

have  never  learned  whether  it  lias  been  done  or  not.  It  was  evi- 
dent that  if  the  already  enlarged  heart  was  to  have  room  in  the 
thorax  for  further  increase  of  its  compensatory  hypertrophy  the 
capacity  of  the  chest  would  have  to  be  augmented.  Accordingly, 
his  attendant,  an  intelligent  trained  nurse,  was  instructed  how  to 
give  resistance  gymnastics  and  breathing  exercises.  These  were 
intended  not  alone  to  strengthen  his  heart  and  develop  his  thorax, 
but  also  to  facilitate  blood-flow  by  better  asj^iration  up  out  of  the 
congested  liver  and  abdominal  vessels.  A  highly  gratifying  expe- 
rience in  other  cases  had  already  shown  how  effective  and  bene- 
ficial such  exercises  are  in  such  a  condition. 

In  addition,  improved  nutrition  was  sought  to  be  achieved 
through  a  dietary  suited  to  his  blood-state  and  to  his  feeble  digest- 
ive and  assimilative  processes.  Starches  and  sugars  were  greatly 
though  not  entirely  cut  off,  such  as  were  allowed  being  carefully 
selected — zwieback,  toast,  a  little  baked  potato,  etc.  Meat  and 
eggs  were  allowed  in  moderate  amounts,  and  certain  fresh  vege- 
tables and  fruits  were  added  to  the  diet  list.  Such  medicinal 
remedies  as  would  aid  digestion,  keep  down  fermentation,  and 
unload  the  portal  vessels  were  prescribed.  To  the  last  end  calo- 
mel was  the  drug  selected,  care  being  taken  not  to  produce  a  too 
powerful  purgative  effect.  Cardiac  tonics,  digitalis  and  strych- 
nine, were  a  minor  part  of  the  treatment,  being  administered  in 
such  doses  only  as  would  gradually  tone  up  the  heart.  Some  im- 
provement began  to  be  apparent  almost  directly,  but  the  family 
removed  to  the  East  before  time  was  afforded  to  observe  the  ulti- 
mate results.  Information  came  to  me,  however,  some  weeks  sub- 
sequently that  the  plan  of  management  detailed  was  bringing 
about  improvement.     I  have  not  seen  the  patient  since  that  time. 

W.  H.  W.,  aged  thirty-nine  years,  male,  physician,  consulted 
me  in  August,  1896,  on  account  of  an  attack  of  mild  articular 
rheumatism,  one  week  previously,  in  right  knee  and  both  hips. 
He  gave  a  history  of  inflammatory  rheumatism  at  age  of  nine  or 
ten,  at  fifteen  remembers  he  had  shortness  of  breath,  and  thinks 
he  had  intermittence.  In  1880  valvular  disease  was  diagnosti- 
cated. During  1895  he  had  an  afternoon  temperature  from  99° 
to  100°  F.,  but  the  cause  was  not  discovered.  In  December,  1895, 
had  a  fever  of  103°  F.  that  lasted  three  days,  and  yielded  to  rest 
in  bed  and  milk  diet.  Afterward  felt  better  than  before.  His 
30 


442  DISEASES  OP  THE  HEART 

condition  was  good  the  following  winter,  and  until  his  recent  in- 
flammatory attack  he  has  attended  quite  constantly  to  an  exact- 
ing general  practice.  At  the  date  of  my  examination  there  was 
slight  dizziness  on  walking,  temperature  at  3  p.  m.  was  99,8°  F., 
pulse  was  98,  sitting,  falling  to  94  on  assuming  the  dorsal  decu- 
bitus, and  was  collapsing ;  capillary  pulse  was  present,  and  there 
was  a  systolic  snap  in  the  femoral  artery.  The  broad,  strong 
apex-beat  was  in  the  sixth  left  interspace,  3^  inches  to  left  of 
sternum,  and  there  was  a  diffused  systolic  impulse  over  the  body 
of  heart  to  left  of  the  breastbone.  First  sound  at  apex  was  pro- 
longed and  impure,  suggesting  a  presystolic  murmur,-  while  the 
aortic  second  was  muffled.  In  the  aortic  area  was  a  soft,  faint 
diastolic  murmur,  transmitted  downward  and  to  the  left.  The 
diagnosis  was  plainly  an  aortic  insufficiency  of  rheumatic  origin, 
and  a  still  persisting  mild  rheumatism. 

He  was  advised  to  give  up  active  exercise  so  long  as  any  trace 
of  joint  inflammation  persisted,  and  to  take  salicylate  of '  soda 
with  small  not  frequent  doses  of  digitalis.  The  patient  subse- 
quently reported  his  recovery  and  return  to  practice.  During  the 
ensuing  three  years  he  abandoned  general  practice  and  limited 
himself  to  ofiice  work;  he  moved  his  residence  a  short  distance 
out  of  the  city,  which  necessitated  travelling  to  and  fro  on  an  ele- 
vated road,  and  the  ascending  of  long,  steep  stairs  to  the  stations. 
He  consulted  me  several  times,  and  on  one  occasion  reported  an 
attack  of  hamioptysis  following  some  exertion.  After  that  attack 
I  confined  him  to  bcnl  for  a  week  or  so,  and  put  him  on  digitalis, 
strychnine,  and  a  vaso-dilator.  He  quite  frequently  experienced 
intermittence  of  the  pulse  for  days  together,  and  as  he  had  some 
digestive  disturbance  at  those  times,  it  was  thought  the  intermis- 
sions were  due  to  that  cause.  On  one  occasion,  in  the  latter  part 
of  1898  or  the  beginning  of  1899,  he  was  suddenly  seized  with 
partial  syncope  while  at  work  over  a  patient  in  his  office,  which, 
however,  was  recovered  from  after  a  few  days  rest  at  home,  with 
the  use  of  digitalis  and  nitroglycerin. 

At  length,  in  January,  1900,  he  entered  my  office  one  morning 
saying  he  had  just  had  a  quite  profuse  hiiemoptysis  without  the 
provocation  of  unusual  physical  effort.  The  heart  was  liurried 
and  occasionally  intermittent;  its  left  border  was  much  outside  of 
the   left   nipple,    its   apex    rather   too   rounded,    and    its   impulse 


THE  TREATMENT  OP   VALVULAR  HEART-DISEASE         443 

not  well  defined.  It  was  also  noted  that  a  rough  systolic  murmur 
had  developed  in  the  aortic  area,  which  had  not  existed  a  year  or 
two  previously.  The  condition  was  considered  very  threatening, 
as  the  haemoptysis  pointed  to  pulmonary  congestion  in  conse- 
quence of  temporary  inadequacy  of  the  left  ventricle.  The  em- 
phatic admonition  was  given  him  to  return  home  at  once  and  go 
to  bed  for  an  indefinite  time,  probably  many  months.  The  advice 
was  acted  on,  and  he  began  the  regular  employment  of  small, 
thrice  daily,  doses  of  tincture  of  digitalis,  with  3  grains  of  potas- 
sium iodide  t.  i.  d.,  and  strychnine;  glonoin  was  substituted  now 
and  then  for  the  iodide. 

His  dietary  was  light  yet  nutritious,  and  the  bowels  were  kept 
free  by  calomel  and  other  laxatives,  as  occasion  required.  For  a 
short  period  he  had  a  light  run  of  fever,  with  vague  joint  pains, 
which  yielded  to  salicylates.  His  cardiac  action  was  invariably 
irregular  after  breakfast,  but  subsequently  grew  less  annoying  or 
disappeared  entirely  after  his  morning  glass  of  milk  was  aban- 
doned, and  his  early  meal  was  made  more  substantial.  This 
patient  remained  in  bed  for  four  months,  at  the  end  of  which 
time  his  heart  was  found  to  have  retracted  somewhat  in  size, 
gained  in  the  force  and  concentration  of  its  apex-beat,  and  had 
become  noticeably  steadier  in  action.  He  was  then  permitted  to 
resume  exercise  very  gradually,  at  first  about  his  room,  and  thus 
by  slow  degrees  to  accustom  himself  to  his  ordinary  habits  of 
life.  When  at  length  he  had  grown  able  to  get  about  as  before 
his  illness,  he  went  into  the  country,  and  there,  driving  about 
with  a  medical  friend,  soon  got  to  feeling  as  well  as  usual.  Small 
doses  of  digitalis  and  strychnine  were  continued  after  he  left 
his  bed  and  resumed  walking,  for  the  purpose  of  maintaining 
what  the  heart  had  gained  by  the  prolonged  rest.  Considering  the 
age  of  this  patient  (now  forty-three)  and  his  history  of  repeated 
subacute  rheumatism  and  probable  aggravation  of  the  endocarditic 
changes,  the  results  secured  were  highly  gratifying,  and  illustrate 
the  immense  value  of  physical  inaction  in  the  recumbent  posture 
in  cases  of  aortic  regurgitation  with  breaking  compensation.  This 
patient  has  had  no  return  of  his  symptoms,  so  far  as  I  have 
learned,  up  to  the  present  writing,  l^evertheless,  the  prognosis 
is  not  encouraging,  for  unless  the  doctor  is  very  careful  a  final  and 
irretrievable  breakdown  is  likely  to  occur  at  any  time. 


iU  DISEASES  OF  THE  HEART 

Medicinal  Agents. — From  the  narration  of  the  foregoing  cases 
it  becomes  apparent  that  the  principle  of  management  applicable 
to  the  stage  of  compensation  does  not  obtain  when  heart-power 
shows  signs  of  failure.  In  this  stage  digitalis  or  one  of  its  con- 
geners is  generally  of  great  service,  and  is  often  indispensable 
for  the  remainder  of  the  patient's  life.  Foxglove  is  incomparably 
superior  to  all  cardiac  tonics  of  its  class,  and  should  always  be 
preferred  so  long  as  vascular  changes  are  not  present  and  when  it 
does  not  disagree  with  the  stomach.  The  former  objection  does 
not  exist  in  the  young  and  in  some  persons  at  or  past  middle  age, 
"When  the  arteries  are  stiff  and  the  vaso-constrictor  effect  of  digi- 
talis is  likely  to  occasion  injurious  rise  of  blood-pressure,  this 
effect  can  be  overcome  by  the  administration  of  -j-^^  of  nitroglyc- 
erin every  two  or  three  hours  in  the  form  of  a  tablet  of  required 
strengtii  or  a  minim  of  the  official  solution.  Two  or  three  grains 
of  an  iodide  salt  are  said  to  accomplish  the  same  purpose,  and 
may  be  administered  three  times  a  day.  If  strophanthus  is  em- 
ployed instead  of  digitalis,  a  vaso-dilator  may  or  may  not  be  neces- 
sary, according  to  the  degree  of  vascular  tension.  The  unpleasant 
effect  of  digitalis  on  the  stomach  is  said  to  reside  in  a  free-fat  and 
certain  narcotic  principles,  the  irritating  qualities  of  the  drug  in 
free  acids,  all  of  which  can  be  removed  without  impairing  its  effi- 
ciency. The  method  of  removing  these  objectionable  constituents 
was  announced  in  1899  by  Dr.  England,  the  chemist  of  the  Phila- 
delphia Hospital.  Accordingly,  such  a  fat-free  tincture  of  digi- 
talis is  now  prepared  by  several  manufacturers  of  pharmaceutical 
preparations,  which  has  been  found  to  possess  equal  if  not  greater 
potency  than  the  tinctures  ordinarily  in  use.  In  most  cases  of  the 
kind  now  under  consideration  digitalis  is  needed  for  its  tonic 
effect,  not  as  a  diuretic,  and  therefore  the  dose  may  be  a  moderate 
one — 5,  10,  or  15  drops  of  the  tincture  once,  twice,  or  thrice  daily, 
as  the  case  may  be.  The  length  of  time  during  which  digitalis  is 
to  be  administered  is  also  variable.  Usually,  hoAvever,  it  will  be 
required  for  many  weeks  or  even  months;  in  grave  cases  it  may 
even  be  coiilinucd  for  the  rest  of  the  patient's  life.  I  am  con- 
vinced that  a  digitalis-habit  may  be  acquired,  yet  see  no  objec- 
tion to  this  .so  long  as  the  continued  use  of  the  remedy  prevents  a 
total  loss  of  compensation. 

xlncther  medicinal  agent  of  generally  recognised  value  as  a 


THE  TREATMENT  OP  VALVULAR  HEART-DISEASE         445 

cardiac  tonic  is  strychnine.  It  stimulates  the  heart  through  its 
action  on  the  cardiac  motor  ganglia.  The  slight  retardation  of  the 
pulse-rate,  which  is  produced  by  its  stimulation  of  the  inhibitory 
apparatus,  is  transient,  and  therefore  not  to  be  reckoned  with  in 
considering  its  therapeutic  influence.  The  increase  of  arterial 
tension,  said  to  result  from  its  stimulation  of  the  vaso-motor  cen- 
tres, is  so  slight  that  opinions  are  at  variance  on  this  point.  This 
effect  is  certainly  too  trifling  to  prove  an  objection  to  its  employ- 
ment, even  in  cases  showing  pronounced  vascular  degeneration 
and  consequent  high  and  sustained  pulse-tension.  The  question 
of  prime  importance  is,  In  what  dose  is  strychnine  to  be  admin- 
istered ?  Believing  that  if  it  stimulates  cardiac  contractions  in 
small  doses  through  its  action  on  the  motor  ganglia,  it  ought  to 
do  this  still  more  powerfully  in  large  ones,  I  have  been  in  the 
habit  of  ordering  doses  that  to  many  seem  dangerous — that  is,  I 
have  many  times  prescribed  g^j-  of  a  grain  hypodermically  every 
three,  and  even  every  two,  hours,  until  seven  or  even  eight  injections 
have  been  given  in  a  day,  and  have  continued  these  doses  for  days, 
and  even  weeks  together  without  ill  effects,  so  far  as  I  could  dis- 
cover. On  the  contrary,  they  have  seemed  to  be  of  positive  bene- 
fit. Indeed,  I  may  say  it  never  occurred  to  me  that  the  remedy, 
even  in  these  doses,  could  do  more  harm  than  occasion  the  primary 
phenomena  of  its  physiological  effect.  As  I  have  but  rarely 
observed  twitchings  to  result,  and  in  these  cases  have  promptly 
discontinued  the  drug;  I  have  not  thought  to  question  its  beneficial 
action.  In  a  recent  conversation  with  Dr.  R.  G.  Curtin,  of  Phila- 
delphia, I  was  surprised  to  find  that  he  strenuously  objects  to 
such  large  doses  on  the  ground  that  it  is  likely  to  produce  short 
and  irritable  systoles  instead  of  long  and  strong  contractions  of 
the  ventricle,  such  as  are  required  to  drive  the  blood  onward  ener- 
getically. He  thinks  that  the  neurility  of  the  cardiac  nerves  and 
ganglia  become  exhausted.  He  stated,  moreover,  that  he  was 
gratified  to  find,  during  a  recent  visit  abroad,  that  such  experi- 
enced clinicians  as  Ernest  Sansom  and  Lauder-Brunton  do  not 
exhibit  the  agent  in  large  doses,  contenting  themselves  in  fact 
with  -g^o  of  a  grain  three  or  four  times  daily.  Such  opinions 
are  worthy  of  consideration,  and  are  here  given  in  the  hope  of 
stimulating  original  observation  on  this  point.  It  is  difficult  to 
abandon  notions  that  have  dominated  one  for  many  years  and 


446  DISEASES  OP  THE  HEART 

seem  to  have  the  support  of  favoiirable  experience.  I  feel  sure 
that  under  the  influence  of  such  large  and  frequently  repeated 
doses  I  have  seen  a  weak  heart  rally  and  evince  signs  of  aug- 
mented power.  I  have  certainly  known  a  dying  heart  to  be  kept 
beating  for  hours  and  days  by  the  combined  use  of  strychnine  and 
nitroglycerin  after  speedy  death  seemed  inevitable.  There  can 
be  no  doubt  of  patients  becoming  so  dependent  upon  this  medi- 
cine, when  taken  for  a  long  period,  that  they  develop  a  strychnine 
habit,  the  same  as  a  morphine  habit.  Only  the  former  is  not  so 
harmful  nor  so  difficult  of  abandonment. 

Whatever  may  be  the  answer  to  this  question  of  large  or  small 
dosage  in  cases  of  dire  urgency,  I  would  not  wish  to  be  thought 
to  advise  them  when  cardiac  power  is  only  beginning  to  fail  or 
cannot  be  said  to  be  entirely  competent.  In  the  stage  now  con- 
sidered it  would  probably  suffice  to  prescribe  ^  or  at  most  ^^ 
thrice  daily.  The  length  of  time  during  which  this  agent  is  to 
be  continued  must  depend  upon  the  circumstances  of  each  case, 
and  therefore  is  to  be  left  to  the  judgment  of  the  medical 
attendant. 

The  value  of  the  nitrite  compounds  has  already  been  stated  in 
speaking  of  the  vaso-constrictor  effect  of  digitalis.  It  may  be  said 
in  addition  that  these  agents  are  often  highly  beneficial  in  the 
treatment  of  aortic  regurgitation  even  when  digitalis  is  not  indi- 
cated. The  earliest  premonition  of  failing  heart-power  in  these 
cases  is  sometimes  shown  by  attacks  of  vertigo,  and  occasionally 
by  syncope,  in  other  instances  by  a  "  pounding  action  of  the 
heart,"  to  quote  the  language  of  the  patients.  These  symptoms 
are  an  indication  that  arterial  tension  is  outstripping  the  contract- 
ing force  of  the  left  ventricle,  which  is  consequently  unable  to  suc- 
cessfully cope  with  the  heightened  peripheral  resistance.  Digi- 
talis augments  the  vigour  of  cardiac  systole,  but  it  also  still  fur- 
ther raises  arterial  tension,  and  hence  may  increase  rather  than 
lessen  the  tendency  to  palpitation.  It  is  better,  therefore,  to  try 
the  effect  of  ^iu)  or  it  may  be  less  of  nitroglycerin  three  to  four 
times  daily  for  the  removal  or  reduction  of  undue  vascular  ten- 
sion, in  the  hope  that  the  symptoms  will  disappear  without  re- 
course to  digitalis  or  strophanthus.  Glonoin  stimulates  the  heart 
only  indirectly  by  causing  vaso-dilatation,  and  thus  removing  ob- 
stacles in  its  path,  so  to  s])eak.     Exce])ting,  therefore,  as  a  vase- 


THE  TREATMENT  OF  VALVULAR  HEART-DISEASE         447 

dilator,  nitroglycerin  is  rarely  to  be  employed  in  this  stage  of 
valvular  affections. 

A  perusal  of  the  cases  narrated  in  this  chapter  will  impress 
the  reader  with  the  great  benefit  often  derived  from  cathartic 
remedies,  and  the  important  role  played  by  them  in  the  manage- 
ment of  patients.  Their  utility  was  first  really  impressed  upon 
me  by  the  writings  of  English  authors,  and  to  their  teachings  I 
owe  much  of  my  success  in  the  management  of  cardiopathies.  I 
shall  have  more  to  say  on  this  subject  farther  on.  It  will  suffice 
at  this  time  to  direct  attention  to  the  tendency  of  most  valvular 
lesions,  especially  mitral  and  those  of  the  right  heart,  to  conges- 
tion of  the  veins  of  the  abdominal  viscera  even  before  signs  of 
compensatory  disturbance  grow  pronounced.  These  congestions 
cannot  be  so  surely  and  quickly  relieved  by  any  other  means ; 
often  they  cannot  be  removed  at  all  without  recourse  to  purga- 
tives. 

If  all  that  was  needed  was  to  increase  the  driving  force  of  the 
left  ventricle,  and  thus  to  push  the  venous  blood  onward,  then 
digitalis  would  be  the  remedy  par  excellence.  In  these  valvular 
diseases,  however,  there  is  an  impediment  to  the  flow  of  venous — 
i.  e.,  of  the  return  blood  through  the  lungs  and  heart.  Behind  this 
impediment  the  circulation  becomes  dammed  up.  The  surest 
mode  of  preventing  an  inundation  is  to  provide  an  outlet,  and  this 
is  done  by  carrying  off  some  of  the  water  of  the  blood  through 
the  intestines.  When  this  has  once  been  accomplished,  then  a 
heart-tonic  or  stimulant  may  be  able  to  reinstate  a  satisfactory 
degree  of  circulatory  equilibrium.  In  some  cases  it  is  impossible 
to  do  more,  or  even  hope  to  do  more,  than  keep  the  stasis  within 
bounds  and  render  the  heart's  labour  somewhat  easier.  Aloes, 
cascara,  etc.,  which  unload  the  colon  relieve  constipation  when  it 
exists,  but  they  do  not  occasion  free  watery  stools,  such  as  are 
needed  to  deplete  the  engorged  portal  and  tributary  veins.  To 
this  end,  saline  preparations  or  such  other  drugs  as  are  not  too 
drastic  are  required.  Of  these,  nothing  is  more  efficient  than 
sulphate  of  magnesia  in  saturated  solution  or  dissolved  in  hot 
water  and  taken  half  an  hour  before  breakfast.  Its  taste  is  very 
objectionable  to  some  persons,  and  it  is  sometimes  rejected  by  a 
sensitive  stomach.  In  such  an  event  it  is  better  tolerated  if  to  it 
are  added  half  a  dozen  minims  of  the  ordinary  essence  of  ginger 


448  DISEASES   OF  THE   HEART 

kept  in  every  hoiiseliolJ.  Four  ounces  of  the  compound  infusion 
of  senna,  the  familiar  "  black  draught "  of  the  English,  make  a 
very  potent  and  not  especially  disagreeable  hydragogue  cathartic. 
Pulvis  jalapi  compositus  is  also  highly  efficient,  and  by  me  greatly 
esteemed.  A  teaspoonful  may  be  taken  by  the  average  individ- 
ual, whose  venous  stasis  is  pronounced,  without  his  being  unduly 
weakened  thereby.  There  are  many  other  remedies  having  a  simi- 
lar action,  of  which  space  forbids  mention. 

Of  all,  however,  there  is  nothing  which  will  ordinarily  pro- 
duce such  happy  results  as  calomel  or  blue  pill.  That  they  power- 
fully affect  the  circulation  and  promote  excretion  is  shown  by 
the  diuresis  they  promote  even  before  they  ■  have  emptied  the 
bowel.  It  is  generally  well  to  administer  the  mercurial  at  bed- 
time, and  have  it  followed  next  morning  by  a  saline.  The  fre- 
quency with  Avhieh  such  cathartic  medication  is  to  be  employed 
will  have  to  be  determined  by  the  degree  of  stasis  and  the  diminu- 
tion that  ensues. 

Patients  with  valvular  disease  are  often  ansemic,  either  be- 
cause the  liver  is  unable  to  utilize  nucleo-albumins  in  the  manu- 
facture of  iron,  or  in  consequence  of  the  destruction  of  haemo- 
globin by  some  ferment  generated  in  the  intestines.  The  so-called 
ha'matics,  iron,  arsenic,  and  the  hypophosphites,  w'ould  appear  to 
be  indicated,  therefore,  and  certainly  do  act  as  a  tonic,  but  to  my 
mind  it  is  doubtful  whether  their  beneficial  effect  is  not  due  to 
their  improving  appetite  and  digestion  rather  than  to  their 
directly  increasing  the  percentage  of  hemoglobin. 

Medicines  that  always  appear  to  me  to  be  of  positive  utility 
are  all  those  that  facilitate  the  better  digestion  of  food  and  lessen 
the  likelihood  of  gastro-intestinal  fermentation.  These  are  pep- 
sin, pancreatin,  taka-diastase,  dilute  hydrochloric  acid,  the  sim- 
ple bitters,  and  the  various  antiseptic  remedies,  salol,  salophen, 
benzonaphthol,  etc.  The  use  of  these  agents,  together  with 
the  improved  function  of  the  digestive  organs  incident  to  the  re- 
lief of  stasis  by  catharsis,  has  always  seemed  to  me  to  do  more 
towards  the  lessening  of  the  spana^mia  than  do  iron  and  arsenic. 

Rest. — Leaving  now  the  consideration  of  medicinal  remedies, 
we  come  to  certain  other  factors  that  are  of  utmost  importance  in 
the  restoration  of  compensation,  and  of  these  rest  takes  the  first 
place.    It  is  universally  recognised  by  practitioners  that  for  weak- 


THE  TREATMENT  OP  VALVULAR  HEART-DISEASE  440 

ened  hearts  no  measure  is  so  beneficial  as  physical  repose  in  the 
recumbent  position.  JNTot  so  with  the  laity,  and  patients  fre- 
quently persevere  with  some  form  of  exercise  in  the  mistaken 
notion  that  thereby  they  will  regain  strength.  So  soon  as  a  heart 
that  is  damaged  by  endocardial  disease  exhibits  signs  of  being 
sorely  overtaxed,  physical  exertion  should  be  interdicted  and  the 
patient  put  at  entire  rest  until  conditions  are  improved.  The  rea- 
sons for  this  are  not  far  to  seek,  being  found  in  the  mechanical 
effect  on  the  circulation  and  in  the  resulting  improvement  to  car- 
diac nutrition. 

When  in  valvular  disease  compensation  is  imperfect,  absolute 
physical  rest  for  several  weeks  seldom  fails  to  prove  highly  benefi- 
cial. The  heart  is  not  compensating,  because  it  is  being  overtaxed 
by  having  to  receive  and  discharge  more  blood  than  it  can  handle 
easily.  If  in  such  a  case  the  patient  is  put  to  rest,  active  muscular 
movements  are  abolished  and  respiration  is  less  rapid  and  more 
shallow.  Venous  blood  is  delivered  to  the  right  auricle  less  rap- 
idly and  the  right  ventricle  is  given  less  work  to  do.  Cardiac 
contractions  become  less  frequent,  but  more  efficient,  and  its  cham- 
bers are  better  able  to  empty  themselves.  Thus  the  decreased 
inflow  and  the  increased  outflow  tend  to  diminish  dilatation  and 
promote  the  re-establishment  of  that  preponderating  hypertrophy 
essential  to  compensation.  Improvement  of  circulation  is  shown 
by  the  better  quality  and  rhythm  of  the  pulse,  by  the  reduction 
of  signs  of  stasis,  and  by  augmented  excretion  of  urine.  There  is 
improved  visceral  function  in  general,  and  there  is  better  nutri- 
tion of  the  whole  body  as  well  as  of  the  heart-muscle.  This  latter, 
which  is  of  great  importance  if  cardiac  power  is  to  be  maintained, 
also  results  directly  from  the  fact  that  physical  repose  favours  a 
better  coronary  circulation. 

With  the  slower  action  induced  by  physical  inactivity  the 
heart  tends  to  gain  in  power,  and  the  left  ventricle  to  discharge  a 
greater  blood-wave  into  the  aorta.  The  coronary  arteries  are  bet- 
ter filled,  and  the  heart-muscle  receives  a  supply  of  blood  more 
adequate  to  its  needs.  This,  however,  is  but  a  part  of  the  benefit 
to  the  heart  proceeding  from  enforced  rest,  particularly  in  cases 
of  mitral  and  aortic  obstruction.  It  has  been  explained  how  this 
treatment  lessens  cardiac  dilatation.  It  is  the  right  heart  chiefly 
that  profits  in  this  way,  the  ventricle  emptying  its  contents  more 


450  DISEASES  OF  THE  HEART 

completely,  and  stasis  in  the  auricle  being  diminished.  This  now 
acts  favourably  on  the  circulation  in  the  coronary  veins.  With 
lessened  intra-auricular  blood-pressure  resistance  to  the  outflow 
from  them  is  less,  owing  to  the  fact  that  they  empty  into  this 
auricle.  Stasis  within  them  tends  to  subside,  and  with  a  better 
circulation  the  products  of  cardiac  metabolism  are  more  fully 
removed. 

Let  us  now  consider  the  benefit  resulting  from  rest  in  the  indi- 
vidual valve-lesions  of  the  left  heart.  In  mitral  stenosis  there  is 
practically  a  dam  built  across  the  blood-stream  at  the  point  where 
the  blood  coming  from  the  lungs  is  poured  into  the  left  ventricle. 
So  long  as  compensation  exists  the  hypertrophied  left  auricle  and 
right  ventricle  arc  a])le  to  discharge  over  this  pathological  dam — 
that  is,  through  the  narrowed  mitral  ojiening — so  large  a  portion 
of  the  blood  sent  through  the  lungs  that  serious  congestion  within 
the  pulmonary  vessels  does  not  take  place.  When  compensation 
begins  to  fail,  and  cardiac  contractions  to  grow  more  rapid,  the 
diastolic  pause,  during  which  the  left  ventricle  is  expected  to  fill, 
is  shortened,  and  time  is  not  allowed  for  the  left  auricle  to  empty 
its  contents. 

Stasis  begins  in  the  parts  back  of  the  stenosis,  and  grows  ever 
greater  with  the  progressing  loss  of  compensation.  Something 
must  be  done  to  diminish  the  rapidity  and  volume  of  the  stream 
pouring  into  the  left  auricle.  This  is  precisely  what  is  accom- 
plished by  rest.  Diastoles  are  lengthened,  more  time  is  given  for 
the  filling  of  the  left  ventricle,  which  consequently  throws  a  larger 
quantity  of  blood  into  the  arterial  system,  and  there  is  a  tendency 
to  restoration  of  the  proper  balance  between  the  aortic  and  pul- 
monic systems,  on  the  one  hand,  and  the  great  arterial  and  venous 
systems  on  the  other. 

In  mitral  incompetence  there  is  a  systolic  reflux  into  the  left 
auricle,  and  the  stream  entering  this  chamber  from  the  lungs  is 
momentarily  checked,  to  be  the  next  instant  unimpeded  as  diastole 
succeds  systole  and  the  blood  gushes  into  the  ventricle.  Yet,  while 
there  is  a  momentary  checking  of  the  flow  in  the  ]uilmonic  vessels 
and  an  in('vitid)l(^  tendency  to  back-i)ressure,  the  column  of  blood 
into  the  left  auricle  and  ])ulnionary  veins,, together  with  the  walls 
of  these  vessels  and  of  the  auricle,  serves  to  resist  the  regurgitant 
rush  from  the  ventricle.     So  long,  therefore,  as  this  resistance  is 


THE  TREATMENT  OP  VaLVULAR  HEART-DISEASE         451 

effectual  cardiac  adequacy  is  uuimpaircd,  and  evidences  of  stasis 
are  wanting. 

When  tliis  compensation  begins  to  fail,  it  is  necessary  to  re- 
lieve the  walls  of  the  left  auricle,  the  pulmonary  vessels,  and  the 
right  ventricle  from  overstrain  by  lessening  the  frequency  of  re- 
gurgitation and  by  retarding  the  flow  from  the  systemic  veins  into 
the  heart  and  lungs.  Rest  accomplishes  this,  and  thus  proves  a 
powerful  factor  in  the  resumption  of  heart-power  and  the  removal 
of  stasis. 

In  the  same  way  also  as  in  mitral  stenosis  the  coronary  veins 
are  better  emptied  and  the  coronary  arteries  are  better  flushed, 
nutrition  of  the  heart-muscle  is  improved,  the  aortic  system  re- 
ceives more  blood  with  each  systole,  and  an  improved  general 
nutrition  results. 

When  in  aortic  obstruction  compensatory  hypertrophy  of  the 
left  ventricle  begins  to  yield  to  dilatation,  the  contents  of  the  ven- 
tricle are  no  longer  adequately  driven  through  the  stenosed  orifice. 
Signs  of  stasis  appear  and  increase  in  proportion  to  loss  of  com- 
pensation. 

_^Two  things  are  now  required  if  the  threatening  breakdown  is 
to  be  averted :  ( 1 )  More  forcible  contractions  on  the  part  of  the 
left  ventricle,  and  (2)  the  delivery  of  less  blood  to  the  ventricle. 
Rest  slows  the  heart  by  lengthening  its  diastoles,  and  but  little  if 
at  all  its  systoles ;  while  if  it  affects  the  vigour  of  the  latter,  it  does 
so  only  indirectly  by  relieving  it  of  strain  and  improving  its  nutri- 
tion. It  can  do  very  little,  therefore,  towards  enabling  the  left 
ventricle  to  drive  blood  through  the  narrowed  aortic  orifice,  and, 
moreover,  experience  has  taught  that  when  in  this  disease  the  left 
ventricle  begins  to  weaken,  it  is  an  indication  that  the  stenosis  has 
overpowered  the  ventricle.  All  that  is  left  is  to  spare  this  cham- 
ber as  far  as  possible.  It  is  by  accomplishing  this,  or  the  second 
requirement  mentioned  above,  that  rest  is  of  service  in  aortic  ste- 
nosis. It  serves  to  retard  the  flow  of  blood  into  the  left  ventricle, 
and  thus  to  lessen  the  amount  which  this  chamber  is  required  to 
discharge  past  the  point  of  constriction.  Therefore,  although  this 
therapeutic  measure  is  of  service  in  conserving  heart-power  in  this 
affection,  it  cannot  accomplish  such  brilliant  results  as  in  mitral 
disease. 

In  aortic  regurgitation  failing  compensation  means  impaired 


452  DISEASES  OP  THE  HEART 

resistance  on  the  part  of  the  left  ventricle  to  the  distending  force 
of  the  regurgitant  stream,  a  still  more  imperfectly  sustained 
blood-pressnre  in  the  arterial  system,  and  after  a  time  secondary 
overfilling  of  the  veins,  right  heart,  and  lungs.  The  danger  lies  in 
sudden  diastolic  arrest  of  the  left  ventricle  while  the  mitral  valve 
is  still  competent,  or  in  such  a  dilatation  of  the  ventricle  that 
relative  mitral  insufficiency  with  all  its  consecutive  evils  is  pro- 
duced. The  yielding  left  ventricle  must  therefore  be  relieved  of 
dangerous  overstrain.  Inasmuch  as  physical  exertion  and  the 
erect  position  are  thought  to  raise  intra-aortic  blood-pressure  and 
intensify  the  regurgitation,  the  removal  of  these  injurious,  even 
dangerous,  influences  becomes  imperative.  This  can  only  be  ac- 
complished by  a  rigid,  and  often  prolonged,  confinement  in  the  re- 
cumbent position. 

There  are  also  two  other  reasons  for  insisting  upon  rest  in 
these  cases:  (1)  Physical  inaction  slows  the  flow  of  blood  in  the 
systemic  veins,  and  thus  tends  to  check  the  discharge  into  the  ven- 
tricle from  the  left  auricle.  With  this  stream,  as  well  as  the  re- 
gurgitant one  reduced,  the  disabled  ventricle  is  called  on  to  handle 
less  blood  and  finds  its  labours  diminished.  (2)  Kest  of  body 
means  also  rest  to  the  heart,  since  by  slowing  down  its  contractions 
its  diastole  or  period  of  repose  is  lengthened,  while  the  actual 
amount  of  work  required  of  it  is  reduced. 

It  may  ])e  argued  that  the  lengthening  of  diastole  favours  a 
better  filling  of  the  ventricle,  and  therefore  compels  it  to  put  forth 
greater  effort  in  order  to  discharge  this  larger  amount  of  blood. 
This  would  be  so  if  the  flow  to  the  left  auricle  were  not  retarded ; 
but  this  latter  being  the  ease,  there  is  not  so  much  likelihood  of 
overfilling  the  ventricle  as  when  the  patient  is  up  and  active.  This 
consideration,  however,  renders  it  probable  that  the  chief  benefit 
of  rest  lies  in  the  rest  to  the  heart-walls  and  in  the  less  forcible 
reflux  from  the  aorta. 

The  mechanical  conditions  existing  in  this  lesion,  and  the 
nature  of  the  patludogical  changes  that  take  place  in  the  myocar- 
dium, render  prognosis  exceedingly  grave  whenever  a  case  of 
aortic  incom])etence  shows  signs  of  failing  compensation.  The 
probability  of  restoring  heart-power  is  so  slight  that  any  means, 
however  unpromising,  should  be  made  the  most  of.  Accordingly, 
rest  of  body  and  mind  must  be  enforced  with  greatest  rigour  and 


THE  TREATMENT  OP  VALVULAR  HEART-DISEASE         453 

for  an  indefinite  length  of  time,  not  merely  for  weeks,  but  for 
many  months.  As  a  matter  of  fact,  the  prospect  of  regaining  car- 
diac power  in  serious  loss  of  compensation  is  poor,  and  rest  is  of 
service  mainly  in  prolonging  life. 

Since,  then,  rest  is  so  valuable  a  means  of  treatment  in  our 
attempt  to  preserve  or  restore  cardiac  adequacy  in  uncompensated 
valvular  disease,  the  physician  must  not  content  himself  with  par- 
tial obedience.  If  the  case  is  urgent,  he  must  see  that  his  orders 
are  carried  out  faithfully.  When  a  patient  is  told  that  rest  in 
bed  is  needed,  he  must  be  made  to  understand  that  by  it  is  meant 
not  rest  for  a  few  hours  each  day,  but  rest  both  day  and  night. 
Moreover,  it  does  not  mean  that  he  can  get  up  as  often  as  he 
pleases  to  fetch  some  article  he  wants  or  to  walk  to  the  toilet,  that 
is  situated  perhaps  a  short  distance  down  the  hall.  It  means  that 
he  is  to  remain  in  bed,  and  is  to  have  the  attention  of  a  nurse  who 
can  spare  him  all  avoidable  effort. 

Patients  suffering  with  aortic  insufficiency  require  more  rigid 
enforcement  of  absolute  rest  than  do  most  persons  with  mitral 
disease.  A  single  indiscreet  effort  may  undo  all  that  has  been 
gained  by  weeks  of  inaction.  Therefore,  such  a  patient  who  is 
struggling  to  preserve  his  left  ventricle  from  complete  destruction 
must  lie  as  quiet  as  possible,  making  use  of  the  bed-pan  and  urinal 
bottle,  and  taking  his  meals  in  the  dorsal  decubitus.  If  this  is 
impossible,  as  is  sometimes  the  case  with  nervous  individuals, 
then  they  may  be  lifted  a  little  higher  by  the  nurse,  and,  sup- 
ported by  pillows,  may  take  their  meals  in  this  position.  Better 
yet  is  the  adjustable  bed,  which  permits  every  possible  position, 
without  the  slightest  exertion  on  the  part  of  the  patient. 

Of  course  each  case  has  to  be  treated  on  its  own  merits  and 
according  to  its  own  exigencies.  One  patient  may  be  permitted 
partial  rest,  and  yet  do  well,  while  another  may  require  the  strict- 
est enforcement  of  this  principle  of  management.  In  some  cases, 
also,  the  attempt  to  carry  out  rigid  confinement  to  bed  for  months, 
no  matter  how  important  it  may  be,  is  sure  to  create  such  a  spirit 
of  restlessness  and  discontent  as  will  counteract  all  that  is  gained 
by  physical  repose.  It  is  evident,  therefore,  that  judgment  and 
tact  are  often  required  in  the  enforcement  of  this  therapeutic 
agency. 

Finally,  when  asked,  as  he  is  sure  to  be,  how  long  rest  is  neces- 


454  DISEASES  OF  THE   HEART 

sary,  the  physician  should  not  bind  himself  to  any  definite  time, 
but  should  let  it  be  determined  by  results. 

Exercise. — When  at  length  under  the  influence  of  enforced 
rest  secondary  congestions  have  been  lessened  or  removed  and 
the  heart  has  regained  a  sufficient  degree  of  strength,  the  patient 
may  be  permitted  to  gradually  resume  exercise.  At  first  he  may 
walk  slowly  and  for  a  brief  period  about  his  room,  care  always 
being  observed  to  avoid  such  a  length  of  walk  as  causes  fatigue, 
or  such  sudden  efforts  as  produce  shortness  of  breath  and  palpi- 
tation. By  degrees  the  walks  may  be  extended  until  the  patient 
is  able  to  leave  the  house  and  stroll  leisurely  in  the  open  air.  He 
must  not,  however,  ascend  stairs  or  hills  until  by  proper  exercise 
on  the  level  his  heart  has  grown  equal  to  the  effort.  Apropos 
of  hill-climbing,  a  word  may  be  said  of  the  Terrain  Cure,  or 
Oertel's  plan  of  having  patients  with  weak  hearts  develop  cardiac 
power  by  ascending  gentle  acclivities.  It  consists  in  having  a 
patient  walk  slowly  up  a  gentle  incline  at  such  a  pace  as  does  not 
occasion  dyspnoea  or  consciousness  of  a  laboured  and  rapid  action 
of  the  heart — infallible  signs  of  cardiac  strain.  Then,  when  an 
ascent  of  a  certain  grade  has  been  mastered,  a  slightly  more  diffi- 
cult slope  is  to  be  attempted  and  overcome  in  the  same  careful 
manner  as  before,  and  thus  paths  of  greater  and  greater  steepness 
are  surmounted.  It  must  always  be  enjoined  upon  the  patient 
that  he  is  to  make  these  ascents  with  great  deliberation,  not  per- 
mitting himself  to  talk  during  such  efforts,  and  stopping  to  rest 
whenever  his  breatliing  grows  short  or  his  heart  begins  to  pound. 
It  is  possible  in  this  manner  for  weakened  hearts  to  attain  much 
greater  endurance,  even  to  develop  hypertrophy.  Experience  has 
demonstrated,  however,  that  it  is  particularly  suited  to  cases  of 
myocardial  weakness  rather  than  of  valvular  disease.  When  a 
mechanical  impediment  to  the  circulation  exists,  as  in  stenosis  or 
regurgitation,  hill-climbing  is  dangerous,  and  patients  are  very 
apt  to  overdo.  Furthermore,  Oertel's  method  has  to  be  very  care- 
fully supervised  if  it  is  to  bring  about  good  and  not  ill  results. 
Consequently,  it  is  but  little  employed  as  compared  with  other 
modes  of  treatment,  and  for  cases  of  uncompensated  valvular 
lesions  is  rarely  advocated. 

The  one  system  involving  ])hysical  exertion  which  gives  the 
best  results,  and  is  adapted  even  to  most  instances  of  uncompen- 


THE  TREATMENT  OP  VALVULAR  HEART-DISEASE         455 

sated  valvular  disease,  is  that  forming  a  part  of  ISTauheim  treat- 
ment, and  which  will  now  be  described. 

Resistance  Exercises. — These  consist  of  voluntary  movements 
by  the  patient  of  flexion,  extension,  and  rotation  of  the  extremi- 
ties and  trunk,  which  efforts  are  carefully  resisted  by  an  attendant 
trained  to  the  work.  Not  only  must  the  attendant  understand 
how  to  resist  the  patient's  movements  without  constricting  the 
part  to  which  he  applies  resistance,  but  he  must  so  adjust  his 
counter-pressure  to  the  patient's  strength  as  to  not  occasion  res- 
piratory or  circulatory  embarrassment.  He  must  therefore  be  suffi- 
ciently skilled  •  to  detect  signs  of  distress  and  to  judge  whether 
too  great  or  too  slight  resistance  is  being  offered. 

The  indications  of  respiratory  and  circulatory  embarrassment, 
for  which  the  attendant  is  to  watch,  are  dilatation  of  the  nostrils 
and  sighing  or  irregular  breathing,  increasing  duskiness  or  pallor 
of  the  countenance,  a  drawn  look  about  the  mouth,  yawning,  per- 
spiration, and  palpitation.  So  soon  as  any  of  these  signs  are  de- 
tected the  movement  is  to  be  stopped  and  the  patient's  extremity 
slowly  allowed  to  assume  a  position  of  rest.  Then,  after  a  suffi- 
cient period  for  repose,  the  exercises  may  be  resumed.  Patients 
are  very  apt  to  hold  the  breath  while  executing  these  movements 
or  to  hold  the  body  rigid,  thus  putting  forth  effort  with  more  than 
the  limb  that  is  being  resisted.  The  attendant  should  therefore 
remind  the  patient  from  time  to  time  to  continue  breathing,  and 
should  see  to  it  that  his  pose  is  easy  and  unconstrained.  Atten- 
tion to  these  points  will  enable  a  patient  to  go  through  the  series 
of  movements  without  fatigue  or  strain.  Furthermore,  the  same 
movement  is  never  to  he  made  twice  in  succession,  and  each  one  is 
to  be  followed  by  a  brief  pause.  It  is  also  well  in  some  cases  to 
allow  the  individual  to  sit  and  rest  occasionally  during  the  treat- 
ment. As  his  endurance  grows,  such  precautions  become  less  and 
less  necessary,  although  the  attendant  must  never  allow  himself  to 
be  thrown  off  his  guard  and  forget  to  maintain  close  watch  of 
the  patient's.. condition.  Many  persons  of  considerable  muscular 
strength  a.^'s  wclined  to  regard  the  exercises  as  too  easy  and  to 
think  no  len  th(t  can  accrue  from  such  gentle  exertions.  They 
consequenStartiant  to  have  more  resistance  offered ;  but  to  all  such 
requests  the-lactendant  must  turn  a  deaf  ear. 

The  last  injunction  to  be  observed  is  to  have  the  movements 


456 


DISEASES  OF  THE   HEART 


made  slowly  and  vnthont  jerldness.  Unsteadiness  of  movement  is 
certain  to  be  produced  if  a  slow  movement,  particularly  of  the  arms, 
is  too  strongly  resisted.  The  object  or  purpose  of  these  exercises 
is  not  to  develop  the  muscles,  but  to  influence  the  heart  and  circu- 
lation ;  all  of  which  is  only  accomplished  when  the  various  move- 
ments are  executed  slowly  and  steadily,  and  the  counter-resistance 
is  accurately  adjusted  to  the  patient's  strength — that  is,  his  car- 
diac not  his  muscular  strength. 

Finally,  the  operator  must  not  grasp  the  patient's  arm,  wrist, 
or  leg,  as  the  case  may  be,  for  this  would  hinder  the  free  play  of 
the  muscles,  but  he  is  to  exert  counter-pressure  or  resistance  by 
placing  the  palmar  surface  of  his  hand  or  fingers  against  that  side 
of  the  patient's  limb  which  looks  in  the  direction  towards  which 

the  extremity  is  to  be  moved.  It 
often  conduces  to  steadiness  of 
movement  for  the  assistant  to 
place  his  other  hand  against  some 
other  part  of  the  limb  or  trunk 
than  that  to  which  resistance  is 
applied.  The  following  descrip- 
tion gives  the  exercises  in  the 
order  in  which  they  are  usually 
executed : 

(1)  The    arms    are    extended 

in  front  of  the  body  on  a  level 

with  the  shoulders  and  with  the 

]ialms    of    the    hands    touching. 

They  are  then  slowly  and  steadily 

moved    outward    until    at    a    line 

with  the  front  of  the  chest,  while 

at   the   same   time   the   attendant 

gently     resists     this     horizontal 

movement.      The    attendant   now 

changes  his  hands,  so  as  to  exert 

pressure  against  the  palmar  surface  of  the  wrists,,   i     the  patient 

slowly  and  steadily  brings  his  arms  back  to  the  poa     .    i  rhence  the 

original  movement  started  (Fig.  84). 

(2)  The  right  arm  hanging  at  the  side,  with  tn  ,  palm  of  the 
hand  forward,  the  forearm  is  slowly  flexed  against  counter-resist- 


Fio.  84. 


THE   TREATMENT   OF   VALVULAR   HEART-DISEASE 


457 


ance  bj  the  attendant  nntil  the  fingers  touch  the  front  of  the 
shoulder.  The  attendant  then  changes  his  point  of  pressure  to 
the  back  of  the  arm,  and  the  extremity  is  slowly  returned  to  its 
former  position  at  the  side  (Fig.  85). 

(3)  This  consists  of  precisely  the  same  movement,  but  exe- 
cuted by  the  left  arm. 

(4)  Both  arms,  depending  at  the  side,  are  slowly  raised  lat- 
erally until  the  thumbs  meet  above  the  head,  and  are  then  brought 
down  to  their  original  position,  these  movements  being  carefully 
resisted  throughout. 

(5)  The  patient  clinches  his  hands  in  the  form  of  a  fist,  but 
with  the  thumbs  extended  upon  the  ulnar  surface  of  the  index 
fingers.  The  tips  of  the  thumbs 
are  then  gently  pressed  together 
in  front  of  the  abdomen,  and, 
a  proper  degree  of  resistance 
being  offered,  they  are  thus  slowly 
raised  until  the  hands  rest  on  the 
top  of  the  head,  after  which  they 
are  slowly  lowered  to  the  original 
position  (Figs.  86  and  87). 

(6)  The  arms,  depending  at 
the  sides,  are  then  elevated  for- 
ward and  upward  without  bend- 
ing them  until  they  are  held  aloft 
on  a  line  with  the  perpendicular 
axis  of  the  body.  They  are  next 
slowly  allowed  to  resume  their 
position  at  the  side  in  the  same 
careful  manner  in  which  they 
were  raised.  To  properly  resist 
this  movement  requires  much 
practice  and  skill,  for  the  reason 

that  the  hand  of  the  attendant  must  be  continually  slipped  around 
the  patient's  wrist  to  suit  the  changing  attitude,  first  to  the  horizon- 
tal and  then  the  vertical  (Figs.  88  and  89). 

(7)  Starting  with  the  arms  hanging  at  the  side,  the  right 
arm  is  slowly  rotated  forward,  upward,  backward,  and  downward 
around  the  shoulder- joint  as  the  pivot,  and  then  in  the  reverse 

31 


Fig.  85. 


Fig.  86. 


Fig.  87. 


Fig.  by. 


THE  TREATMENT   OF  XALVULAR   HEART-DISEASE  459 

direction  until  the  circle  is  completed,  counter-pressure  being  all 
the  time  exerted  by  the  attendant, 

(8)  This  consists  of  a  similar  movement,  executed  by  the  left 
arm.  These  two  movements  are  difficult  both  for  the  patient  and 
the  attendant,  and  should  not  be  given  to  patients  who  are  very 
weak  or  whose  hearts  are  incapable  of  withstanding  much  exer- 
cise. Resistance  to  this  movement  is  likewise  extremely  difficult, 
for  the  reason  that  the  attendant  has  to  change  hands  during  the 
progress  of  the  movement,  yet  without  causing  jerkiness  or  too 
much  interference. 

(9).  The  patient  bends  his  body  forward  at  the  hips  with- 
out flexing  his  knees,  and  then  brings  it  back  to  the  erect 
position,  while  the  attendant,  standing  at  his  side,  resists 
the  forward  movement  by  one  hand  against  the  ujDper  part  of 
the  sternum  and  the  other  in  the  middle  of  the  back,  and  the 
return  movement  of  the  trunk  by  one  hand  against  the  upper 
dorsal  region  and  the  other  upon  the  epigastrium  (Figs.  90 
and  91). 

(10)  Standing  with  the  feet  firmly  planted  upon  the  floor,  the 
patient  rotates  his  trunk  around  its  vertical  axis,  at  first  to  the 
left,  next  to  the  right,  and  then  back,  so  as  to  face  forward,  as 
before  starting.  The  attendant  resists  this  movement  by  placing 
one  hand  against  the  advancing  shoulder  and  the  other  in  the 
opposite  axilla,  and  then  changing  his  hands  as  the  body  is  rotated 
in  the  opposite  direction  (Fig.  92). 

(11)  In  this  movement  the  trunk  is  bent  laterally,  first  in 
one  direction,  then  in  the  other,  and  lastly  is  brought  at  rest  in 
the  upright  posture.  To  resist  this  flexion  the  attendant  places 
one  hand  on  the  hip  and  the  other  against  the  side  of  the  chest 
towards  which  the  body  is  to  be  bent  (Fig.  93). 

(12)  Both  arms  hanging  at  the  sides,  with  the  palms  facing 
towards  the  thighs,  are  simultaneously  moved  backward  and 
upward  as  far  as  possible  without  bending  the  body,  and  are  then 
brought  down  to  the  sides,  resistance  meanwhile  being  carefully 
exerted  by  the  attendant  (Fig.  94). 

(13)  The  patient  supports  himself  by  resting  one  hand  on  a 
chair,  and  then  raises  the  opposite  leg  as  far  as  possible  in  a  lat- 
eral direction,  while  the  attendant  resists  both  the  upward  and 
the  return  movement  (Figs.  95  and  96). 


Fit*.  90. 


Fii,.  'Jl. 


Fio.  'J2. 


Fio.  'J3. 


460 


Fig.  94. 


Fiii.   H5 


YiG.  i)G. 


Fu..  u: 


461 


Fni.  '.t'j 


I'lo.  101. 


THE  TREATMENT  OF   VALVULAR  HEART-DISEASE         463 


(14)  This  is  the  same  movement,  but  done  with  the  opposite 
extremity. 

^  (15)  Resting  one  hand  on  a  chair,  as  heforo,  the  patient 
extends  his  opposite  leg  and  thigli,  bnt  without  Ixmding  his 
knee,  as  far  forward  and  upward  as  possible,  after  which  the 
extremity  is  slowly  returned  to  its  original  position,  resistance 
to  both  movements  being  offered 
by  the  attendant  (Figs.  07 
and  9S). 

(16)  This  is  a  similar  effort 
put  forth  by  the  opposite  ex- 
tremity. 

(17)  Both  hands  supported 
on  the  back  of  a  chair,  one  leg 
is  flexed  at  ±he  knee  while  re- 
sistance is  offered  by  the  attend- 
ant's hand  placed  at  the  heel. 
The  return  is  resisted  by  the 
hand  against  the  ankle  just 
above  the  instep  (Figs.  99  and 
100). 

(15)  This  is  a  corresponding 
movement  by  the  other  leg,  re- 
sisted in  the  same  manner. 

(19)  Supporting  himself  by 
the  back  of  a  chair  the  patient 
flexes  his  thigh  at  the  hip,  the 

leg  hanging  limp  and  flexed,  wdiile  the  attendant  resists  first  the 
upward  and  then  the  downward  movement  (Figs.  101  and  102). 

(20)  This  is  a  similar  movement  by  the  opposite  thigh. 

If  desired,  additional  movements  of  flexion,  extension,  and 
rotation  of  the  hands  and  feet  may  be  devised.  In  carrying  out 
these  exercises  care  should  be  taken  that  movements  involving 
the  use  of  the  same  groups  of  muscles  do  not  succeed  each  other 
directly,  but  are  interrupted  by  exercises  made  by  different  sets 
of  muscles.  The  purpose  of  this  precaution  is  the  avoidance  of 
undue  muscular  fatigue  of  weak  patients.  Given  with  requisite 
deliberation,  and  with  sufficient  pauses  for  rest  between  move- 
ments, such  a  series  of  resistance  gymnastics  ordinarily  takes  about 


Fig.  102. 


464  DISEASES  OP   THE   HEART 

half  an  hour.  If  after  a  rest  of  ten  to  fifteen  niinntcs  the  i):iticnt 
does  not  feel  or  evince  fatigue,  he  may  then  repeat  the  series. 
Tliey  are  generally  given  daily,  an  hour  or  more  after  a  meal. 
Patients  whose  condition  is  fairly  good  may  be  allowed  to  per- 
form them  twice  a  day — that  is,  in  the  forenoon  and  again  in  the 
afternoon. 

These  exceedingly  simple  exercises  are  a  powerful  agent  for 
good  or  a  means  of  great  harm,  depending  on  the  manner  in  which 
they  are  given  and  the  condition  of  the  heart.  I  do  not  believe 
they  should  be  given  to  patients  whose  compensation  is  wholly 
gone.  In  this  opinion  I  differ,  I  think,  with  Schott  and  Bezly 
Thorne,  who  have  written  so  much  in  praise  of  them.  If  there  is 
pronounced  stenosis  of  an  orifice,  with  great  dilatation  of  the 
chambers  back  of  the  lesion,  harm  may  follow  their  employment, 
the  same  as  with  digitalis  incautiously  given.  This  was  sadly 
illustrated  in  one  of  my  cases.  First  lessen  the  cardiac  inade- 
quacy by  rest  and  other  treatment,  and  then  these  movements  are 
likely  to  prove  highl}^  beneficial.  In  more  than  one  patient,  whose 
enormously  congested  liver  had  refused  to  subside  under  the  free 
and  prolonged  use  of  cathartics  and  heart-tonics,  I  have  seen  the 
organ  diminish  rapidly  in  size  during  the  administration  of  re- 
sistance together  with  breathing  exercises.  It  seemed  as  though 
they  served  to  bring  about  an  aspiration  of  the  blood  out  of  the 
engorged  liver.  They  are  far  superior  to  massage,  which  seems 
to  me  to  i)roduce  just  the  opposite  effect.  Massage  promotes  a 
more  rapid  and  ampler  flow  of  blood  to  the  heart,  while  resist- 
ance movements  ai'c  thought  to  exert  their  salutary  effect  by  dilat- 
ing the  arterioles,  and  thus  unloading  the  overburdened  heart. 

Nauheim  Baths. — The  balneological  treatment  of  heart-disease 
has  not  received  as  much  attention  in  this  country  as  in  Europe, 
and  yet  it  has  been  growing  in  popularity  even  here.  Large  num- 
bers of  wealthy  Americans  and  Englishmen  annually  make  pil- 
grimages to  Germany  for  treatment  at  the  little  resort  known  as 
Bad  Nauheim,  where  the  employment  of  cool  saline  and  efferves- 
cing baths  was  first  introduced  in  this  class  of  affections.  Patients 
of  moderate  means  cannot  afford  so  expensive  a  journey,  and  must 
either  forego  this  treatment  altogether  or  content  themselves  with 
the  use  of  artificially  prepared  waters.  For  tlie  consolation  of 
such  it  may  be  stated  that  amj)le  experience  all  over  the  world,  but 


THE  TREATMENT  OF  VaLVCJLAR  HEART-DISEASE         465 

particularly  in  England,  has  shown  that  equally  efficient  results 
may  be  obtained  in  this  way  as  at  Bad  Nauheim.  I  myself  took 
a  course  of  baths  at  that  resort  in  the  summer  of  1893,  and  ever 
since  my  return  have  been  employing  this  plan  of  treatment  in 
suitable  cases,  and  can  justly  claim  priority  in  this  regard  over  all 
others  in  this  country.  I  have  not  desired  to  make  a  fad  of  this 
treatment,  and  therefore  have  not  subjected  as  many  patients  to 
it  as  might  have  been  done,  but  it  is  within  bounds  to  say  that 
considerably  over  one  hundred  have  thus  been  treated  by  me. 
Some  of  my  patients  have  taken  the  baths  in  Germany,  generally 
after  a  course  in  Chicago,  although  one  has  just  finished  here 
who  has  previously  treid  the  baths  at  Bad  ISTauheim.  All  agree 
in  the  statement  that  the  effects  with  artificial  waters  are  the  same 
as  with  the  natural,  the  chief  and  perhaps  striking  difference 
consisting  in  the  more  powerful  effervescence  of  the  latter,  par- 
ticularly in  the  form  of  the  Sprudel-Strom-Bad  (flowing  effer- 
vescing bath).  Another  advantage  in  favour  of  the  latter  lies  in 
the  consideration  that  when  a  patient  goes  to  Germany  he  leaves 
his  cares  behind  him,  and  while  there  abandons  himself  to  the  one 
purpose  of  getting  well.  On  the  other  hand,  I  have  been  assured 
that,  owing  to  the  immense  number  of  invalids  who  frequent  the 
place,  patients  are  apt  to  miss  the  watchful  care  and  oversight 
which  many  of  them  require  and  receive  at  home. 

The  waters  of  Bad  jSTauheim  are  impregnated  with  various 
chloride  salts,  the  two  to  which  particular  virtue  is  attributed  in 
their  effect  upon  the  circulation  being  the  chlorides  of  sodium  and 
calcium.  In  addition,  the  springs  used  for  the  j)reparation  of  the 
baths  are  highly  charged  with  carbonic  acid,  which  makes  them 
very  stimulating,  particularly  when  used  in  the  form  of  the  flow- 
ing bath — that  is,  with  a  steady  stream  of  effervescing  water 
flowing  over  the  body  of  the  bather  in  the  tub.  This  is  compara- 
tively rarely  prescribed,  being  considered  too  exhilarating  for 
any  except  those  in  fairly  robust  health.  It  is  the  rule  in  the 
employment  of  this  balneological  treatment  to  begin  with  water 
of  a  temperature  of  93°  to  95°  F.,  according  to  the  ability  of  the 
patient  to  react,  and  with  water  containing  1  per  cent  of  sodium 
chloride  and  ^  per  cent  of  calcium  chloride,  but  no  carbonic  acid, 
this  latter  being  added  at  the  end  of  the  second  week,  or  when  a 
temperature  of  91°  to  90°  F.  has  been  attained.     The  duration  of 


466  DISEASES  OF  THE  HEART 

the  first  bath  is  from  five  to  eight  minutes,  depending  upon  the 
strength  and  reaction  of  the  individual.  One  treatment  is  taken 
daily  for  two  or  three  successive  days,  and  then  comes  a  day  of 
rest.  This  is  to  prevent  undue  depression,  as  is  likely  to  be  expe- 
rienced when  no  interruption  in  the  course  of  treatments  occurs. 
The  patient  is  required  to  rest,  by  preference  lying  down,  after 
each  bath,  and  if  reaction  is  not  good  and  prompt  to  take  a  warm 
drink  of  some  kind  and  to  cover  up  warmly.  He  is  also  required 
to  see  his  medical  attendant  daily,  or  as  often  as  the  latter  may 
elect,  that  the  effect  of  the  treatment  may  be  judged  of  and  the 
baths  modified  as  his  progress  requires.  The  principle  underlying 
the  ordering  of  these  is  that  the  percentage  of  the  ingredients  is  to 
be  increased,  the  temperature  lowered,  and  the  duration  length- 
ened until  finally  the  chloride  of  sodium  reaches  3  per  cent,  chlo- 
ride of  calcium  1  per  cent,  the  temperature  87°  or  85°  F.,  and 
the  time  twenty  minutes. 

The  rapidity  with  which  this  change  can  be  effected  depends 
upon .  the  degree  of  objective  and  subjective  improvement  ob- 
served, but  as  a  rule  this  maximum  is  not  attained  under  three  or 
it  may  be  four  weeks.  In  the  more  serious  cases,  or  such  as  ex- 
hibit considerable  anaemia  and  sluggish  reaction,  it  is  not  always 
wise  to  bring  the  temperature  below  89°  or  even  90°  F.,  although 
the  maximum  in  strength  and  duration  may  be  the  same  as  when 
lower  temperatures  are  prescribed.  It  is  not  well  to  reduce  the 
temperature  more  than  a  degree  at  a  time,  and  whenever  this  is 
done  the  proportion  of  the  salts  is  usually  increased.  For  the 
most  part  effervescing  baths  are  ordered  at  the  end  of  ten  days 
or  two  weeks,  or  when  the  higher  percentages  of  salts  have 
been  reached ;  but  if  the  patient  is  inclined  to  chilliness  at  a 
temperature  that  ought  to  produce  at  least  a  tolerable  feeling  of 
warmth,  or  if  afterward  the  extremities  are  cold  and  the  skin 
does  not  get  into  a  good  glow,  it  may  be  well  to  add  the  gas  at  an 
earlier  period.  The  warmer  saline  baths,  95°  to  92°  F.,  are  con- 
sidered soothing,  while  the  cooler  effervescing  ones,  89°  to  85°  F., 
are  stimulating,  and  hence  are  not  applicable  to  very  weak  hearts. 

The  direct  effect  of  each  bath  should  be  to  render  the  pulse 
slower,  of  better  quality,  and  more  regular  if  previously  irregular. 
The  area  of  deep-seated  cardiac  dulness  diminishes  and  the  heart- 
sounds  grow  stronger.     Endocardial  murmurs  intensified  by  dila- 


THE  TREATMENT  OF   VALVLTLAR  HEART-DISEASE         467 

tation  may  become  less  loud,  or  if  weak  from  cardiac  asthenia, 
may  after  the  bath  be  found  to  be  more  intense.  The  degree  of 
benefit  is  to  be  determined  chiefly  by  the  size  of  the  heart  and  by 
the  character  of  its  action.  As  a  rule,  also,  the  patient  is  con- 
scious of  a  sense  of  well-being  and  of  some  lessening  of  whatever 
symptoms  have  annoyed  him. 

If  the  treatment  has  been  judiciously  ordered  and  overseen, 
the  heart  is  found  to  gain  in  strength  week  by  week,  visceral  con- 
gestions diminish,  as  evinced  by  increased  diuresis,  the  colour  of 
the  skin  grows  more  like  that  of  health,  and  the  patient  gradually 
gains  in  vigour  and  ability  to  exercise  without  discomfort. 

Just  how  this  balneological  treatment  brings  about  improve- 
ment is  still  a  matter  of  speculation  and  discussion,  being  by 
Schott  explained  on  the  hypothesis  of  increased  tissue  change 
together  with  a  reflex  stimulation  of  the  heart  Avhicli  causes  its 
slower  and  more  powerful  contractions,  and  with  a  physiological 
stimulation  of  the  arterioles  and  capillaries  by  the  passage  of  the 
gas  and  salts  through  the  skin.  By  others,  in  particular  Broad- 
bent,  the  beneficial  action  of  the  baths  is  attributed  to  dilatation 
of  the  cutaneous  capillaries,  in  consequence  of  which  resistance 
to  the  work  of  the  left  ventricle  is  lessened  and  the  transfer  of 
blood  from  the  venous  to  the  arterial  system  is  promoted.  The 
objection  urged  against  this  explanation  is,  that  the  rate  of  the 
pulse  should  be  increased  rather  than  decreased,  so  that  there 
must  be  some  additional  influence  at  work.  The  following  is  the 
view  of  Medicinalrat  Groedel  of  Bad  jSTauheim :  "  The  incon- 
testable success  which  our  baths  have  on  the  heart's  function  and 
the  entire  circulation  is  only  to  be  explained  if  we  believe  in  a 
direct  action  by  way  of  the  end-organs  of  the  cutaneous  nerves  on 
the  central  vascular  and  cardiac  nervous  system,  both  trophic  and 
motor."  It  may  also  be  stated  that  so  far  as  concerns  the  demon- 
strable effect  of  the  two  means  of  treatment,  the  resistance  gym- 
nastics and  the  baths,  the  results  if  not  the  action  are  identical  in 
diminished  size  of  the  dilated  heart  and  improved  energy  and 
steadiness  of  its  contractions.  Consequently  it  is  customary  at 
Bad  ISlauheim  to  have  the  patient  receive  both  forms  of  treatment 
each  day.  Finally,  it  is  usual  to  send  the  patient  away  at  the 
close  of  a  course  of  baths  for  a  rest  of  a  month  to  six  weeks,  after 
which  he  returns  for  another  course  known  as  the  after-cure. 


468  DISEASES  OF  THE  HEART 

Inasmuch  as  the  effect  on  the  heart  and  cirenhition  of  the  arti- 
ficial and  natural  waters  is  identical,  1  will  now  describe  how  the 
former  are  prejiared.  The  ingredients  required  are  common  salt 
(chloride  of  sodium)  and  chloride  of  calcium,  bicarbonate  of  so- 
dium, and  compressed  tablets  of  acid  sulphate  of  lime.  Instead 
of  these  latter,  commercial  hydrochloric  acid  may  be  used.  The 
first  is  to  be  had  as  ordinary  ''  butter  salt "  of  the  trade,  while 
the  calcium  salt  comes  in  iron  drums  holding  from  600  to  800 
pounds.  This  latter  is,  moreover,  deliquescent,  and,  being  corro- 
sive, is  most  conveniently  kept  in  a  strong  solution  of  definite 
strength.  I  have  it  kept  on  hand  by  one  of  the  Chicago  druggists, 
who  dispenses  it  to  my  patients  on  my  prescriptions.  To  begin 
with,  the  baths  contain  onl}^  these  two  ingredients,  and  are  there- 
fore simple  brine  baths.  It  takes  from  50  to  60  gallons  of  water 
in  an  ordinary-sized  bath-tub  to  immerse  a  person  of  average  size 
up  to  his  neck  when  lying  in  a  semi-recumbent  position.  When  the 
amount  of  water  is  known  it  is  an  easy  matter  to  determine  tHe 
number  of  pounds  of  salt  and  the  number  of  pints  of  calcium- 
chloride  solution  to  be  added.  When  at  length  the  water  is  to  be 
charged  with  carbonic  acid  in  addition,  it  is  done  by  dissolving 
bicarbonate  of  soda,  2  pounds  to  each  bath,  and  the  same  number 
of  ounces  of  commercial  muriatic  acid  or  the  compressed  tablets 
already  mentioned.  The  acid  is  so  corrosive  and  difficult  to  keep 
without  its  fumes  injuring  the  furniture  of  the  bath-room  that  I 
now  order  the  packages  of  "  effervescing  bath  salts  "  manufac- 
tured for  the  purpose  by  two  firms  in  Kew  York  city,  and  which 
are  likewise  kept  in  stock  by  the  Chicago  druggists.  Each  pack- 
age contains  2  pounds  of  soda  and  8  tablets  and  printed  direc- 
tions for  their  use.  One  such  package  is  required  for  a  single 
bath.  These  effervescing  tablets  possess  this  additional  advantage 
over  the  acid,  that  the  evolution  of  gas  is  steady  and  continuous. 
They  are  also,  however,  corrosive,  and  the  bottom  of  the  tub 
should  be  protected  by  a  rubber  sheet. 

It  is  my  custom  to  prescribe  the  baths  in  groups  of  three  with 
the  rest  day  between — that  is,  on  every  fourth  day — and  a  course 
usually  extends  over  a  period  of  six  weeks.  In  most  cases  the 
resistance  exercises  are  also  taken,  l)ut  some  hours  prior  to  or 
after  the  bath,  that  the  effect  on  the  heart  may  be  maintained. 
I  always  strive  to  impress  patients  with  the  importance  of  living 


THE  TREATMENT  OF   VALVULAR  IIEART-DLSEASE  469 

as  quiet  and  routine  a  life  as  possible,  and  in  particular  to  strenu- 
ously avoid  undue  cardiac  strain  that  they  may  not  destroy  the 
benefit  expected  to  be  derived  from  the  treatment, 

I  can  recall  only  5  cases  in  which  this  plan  of  treatment 
seemed  to  do  harm  rather  than  good.  Two  were  instances  of 
chronic  myocarditis,  the  hearts  being  very  dilated  and  their  action 
arrhythmic.  One  was  a  mitral  lesion  with  oedema  and  other  signs 
of  rather  a  badly  destroyed  compensation ;  but  as  this  patient  was 
compelled  to  journey  some  distance  each  day  to  get  his  bath,  it 
may  be  that  the  exertion  thus  required,  and  not  the  treatment,  was 
responsible  for  the  want  of  improvement.  The  remaining  two 
were  cases  of  serious  valvular  disease  complicated  by  pericardial 
adhesions.  In  both,  the  engorgement  of  the  liver  became  mani- 
festly greater  towards  the  termination  than  at  the  commencement 
of  the  course,  and  the  treatment  was  discontinued.  All  other 
patients  have  exhibited  more  or  less  improvement,  while  in  some 
instances  this  has  been  most  gratifying  both  to  the  patient  and 
myself. 

I  am  very  positive  in  my  belief  that  this  treatment  should  not 
be  given  to  persons  whose  compensation  is  wholly  lost,  or  indeed 
seriously  broken,  and  therefore  the  consideration  of  this  measure 
has  been  introduced  in  this  portion  of  the  present  chapter.  I  have 
just  finished  giving  a  course  of  30  baths  to  a  lady  with  a  pure 
mitral  stenosis  who,  when  she  began,  gave  indications  of  failing, 
or  at  least  threatened,  compensation.  The  second  sound  at  the 
heart's  apex  was  wanting,  there  being  only  a  presystolic  murmur 
and  sharp  first  sound.  She  complained  of  much  ill-defined  dis- 
comfort at  the  heart,  and  the  pulse  was  rapid  and  exceedingly 
feeble.  Before  the  course  was  completed  the  second  sound  had 
returned  at  the  apex,  the  area  of  cardiac  dulness  was  distinctly 
smaller,  and  the  pulse  was  slower  and  of  greater  volume.  She 
declared  she  felt  perfectly  well.  In  this  instance,  as  is  often  my 
habit,  I  ordered  the  frequent  use  of  a  laxative  water,  and  for  a 
time  5-drop  doses  of  fat-free  tincture  of  digitalis  thrice,  then 
twice,  and  at  last  but  once  daily.  I  do  this  because  it  has  seemed 
to  me  that  in  this  way  I  have  secured  more  lasting  results. 

Contra-indications  to  the  employment  of  this  balneological 
treatment  are  the  following:  Aortic  aneurysm,  pronounced  and 
extensive  arteriosclerosis,  and,  in  my  opinion,  all  cases  manifest- 


470  DISEASES   OE   THE  HEART 

ing  marked  signs  of  cardiac  inadequacy,  such  as  ascites  and  con- 
siderable dropsy  with  a  greatly  distended  and  feeble  heart,  and 
cases  complicated  by  extensive  mediastinopericardial  adhesions. 
Chronic  renal  disease  does  not  contra-indicate  the  treatment 
unless,  of  course,  it  has  led  to  too  pronounced  a  degree  of  car- 
diac incompetence.  Lastly,  it  may  be  stated  that  if  the  pulse  does 
not  grow  of  better  quality  after  the  bath,  but,  on  the  contrary,  is 
observed  to  become  less  full  and  strong,  the  treatment  will  not 
produce  beneficial  results  and  would  better  be  discontinued. 

Diet. — This  is  a  matter  requiring  in  this  stage  of  valvular 
heart-disease  very  careful  attention,  yet  concerning  which  notions 
are  for  the  most  part  woefully  vague  and  inaccurate.  Physiologi- 
cal chemistry  has  not  yet  worked  out  the  changes  taking  place 
in  the  digestive  process  as  a  result  of  disease.  We  know  that 
the  passive  congestion  of  the  abdominal  organs  produced  by  un- 
compensated cardiac  disease  leads  to  a  chronic  catarrh  of  the 
stonuich  (Einhorn),  with  diminution  and  even  disappearance  of 
the  hydrochloric  acid  (lliifler  and  Jorn),  which,  with  its  im- 
paired motility,  may  seriously  derange  its  function.  Reasoning 
by  analogy,  we  may  also  assume  that  the  pancreatic  and  hepatic 
secretions  are  likewise  altered  in  quantity  and  quality,  or  that  if 
not  secreted  in  less  amounts  they  are  poured  into  the  duodenum 
in  diminished  quantity  in  consequence  of  catarrhal  obstruction 
to  their  outflow.  Just  what  modification  in  the  character  of  the 
pancreatic  juice  takes  j^lace  we  do  not  know,  yet  clinical  obser- 
vation seems  to  warrant  the  inference  that  the  amylopsin  and 
fat-splitting  ferment  are  more  unfavourably  influenced  than  is  the 
proteolytic  ferment. 

Furthermore,  in  consequence  of  sluggish  circulation  in  the 
veins  that  carry  blood  to  the  portal  system,  the  bile  is  absorbed 
slowly  from  the  intestine,  and  when  secreted  is  watery  and  poor  in 
mineral  constituents.  Although  the  secretion  of  bile  is  but  a 
minor  function  of  the  liver,  still  a  deterioration  in  its  quality  and 
diminution  in  its  quantity  must  exert  a  baneful  influence  upon 
intestinal  digestion.  These  theoretic  considerations  are  borne  out 
by  clinical  observations,  for  cardiac  patients  are  very  prone  to 
gaseous  distention  of  the  stonuich  and  intestines  and  to  eructa- 
tions and  other  indications  of  fonuentation  of  the  ingesta.  The 
fatty  acids  thus  engendered  occasion  still  further  irritation  of  the 


THE   TREATMENT   OF  VALVULAR   HEART-DISEASE  471 

stomach  and  establish  a  vicious  circle  which  augments  the  evils 
primarily  attributable  to  disturbed  circulation. 

This  is  not  the  only  aspect  of  the  case.  There  is  alteration  in 
the  metabolic  processes  incident  to  derangement  in  the  blood-sup- 
ply to  the  digestive  and  other  viscera,  while  toxines  are  locally 
developed  which  either  must  be  destroyed  in  the  engorged  and 
functionally  impaired  liver  or  must  pass  through  into  the  general 
blood-stream  and  exert  their  noxious  effects  upon  the  heart  and 
nervous  system.  The  investigations  of  Husche  appear  to  show 
that  the  excretion  of  urea  and  uric  acid  is  altered.  The  retention 
of  the  former  is  variable,  while  the  excretion  of  the  latter  is  hin- 
dered during  disturbance  of  compensation  and  increased  after 
this  has  been  restored. 

It  is  not  strange,  in  the  light  of  the  foregoing  considerations, 
that  some  patients  are  greatly  disturbed  by  fermentative  indiges- 
tion after  the  taking  of  the  simplest  and  most  easily  digested  food. 
Dyspnoea  is  intensified  or  developed,  or  they  are  distressed  by 
palpitation.  Others  are  not  conscious  of  local  disturbance,  but 
complain  of  pains  and  aches,  muscular  stiffness  and  cramps,  nerv- 
ous symptoms,  such  as  despondency,  insomnia,  and  frightful 
dreams,  fidgetiness  of  the  legs,  and  sundry  other  sensations  that 
are  so  commonly  attributed  to  uric-acid  retention.  It  may  be  re- 
marked here,  however,  that  Dr.  Wesener's  researches  appear  to 
show  that  these  constitutional  symptoms,  as  well  as  many  others, 
are  due  not  to  uric  acid,  but  to  indicamiria  and  oxaluria.  One  of 
my  patients  was  greatly  troubled  by  headache,  insomnia,  and 
other  nervous  phenomena,  and  Wesener's  analysis  of  her  urine  col- 
lected at  the  time  showed  an  enormous  excess  of  indican  and 
oxalic  acid.  Thereupon  an  attempt  was  made  to  stop  proteids 
and  administer  carbohydrates  in  the  hope  of  relieving  her  dis- 
tress. It  was  found,  however,  that  at  once  she  began  to  have  so 
much  flatulent  distention  of  the  stomach  and  bowels  with  aggrava- 
tion of  her  dyspnoea  that  the  non-nitrogenous  diet  had  to  be  aban- 
doned for  a  return  to  meats,  etc.,  wdth  all  their  evil  consequences. 

The  problem  of  how  to  pieet  the  food  requirements  of  cardiac 
sufferers  is  a  complex  one  and  most  difficult  of  solution  when  w^e 
have  to  do  with  the  stage  of  imperfect  compensation.  It  is  quite 
generally  agreed  that  in  cases  of  heart-disease  uncomplicated  by 
renal  lesions  the  myocardium  should  be  supplied  with  a  relatively 


4Y2  DISEASES   OP   THE   HEART 

large  proportion  of  proteids.  The  main  reason  for  this  lies  in  the 
fact  that  the  nitrogenous  principles  are  tissne-forniing,  and  hence 
reparative  elements  of  the  dietary,  and  should  be  in  excess  when- 
ever there  is  a  demand  for  increased  muscular  work,  as  is  the  case 
in  cardiac  affections,  ^loreover,  meats  and  other  foods  rich  in 
proteids  do  not  undergo  the  same  sort  of  fermentation  and  gen- 
erate so  much  gas  as  do  earholivdrates,  and  do  not  so  injuriously 
distend  the  hollow  abdominal  viscera.  They  are  not  so  bulky,  and 
therefore,  relatively  to  the  quantity  ingested,  contain  a  far  larger 
proportion  of  nutrient  material.  For  obvious  reasons  persons 
with  uncompensated  valvular  lesions  should  have  their  dietary 
definitely  ordered  and  carefully  supervised'  by  their  medical 
attendants. 

It  should  be  remembered  that  digestion  and  assimilation  are 
both  slow,  and  therefore  the  first  rule  to  be  laid  down  is  that  food 
is  not  to  he  taken  at  short  intervals,  but  ample  time  allowed  for 
the  stomach  to  empty  itself  before  fresh  nourishment  is  adminis- 
tered. The  fatty  acids  and  other  irritating  products  of  fermenta- 
tion often  occasion  a  feeling  of  faintness  or  gnawing  at  the  epi- 
gastrium which  is  mistaken  for  hunger  and  thought  to  indicate 
a  need  for  more  food.  In  other  cases  appetite  is  poor  and  patients 
are  unable  to  eat  heartily  at  the  regular  meal-hours,  and  hence  the 
friends  and  even  the  physician  get  the  idea  that  the  meals  must 
be  re-enforced  by  milk,  egg-nog,  etc.,  midway  between.  I  have 
thus  known  nourishment  to  be  administered  every  two  or  three 
hours.  Sucli  is  undoubtedly  a  mistake.  The  congested  and  per- 
haps ocdematous  walls  of  the  stomach  cannot  by  energetic  peristal- 
sis empty  the  chyme  into  the  duodenum  as  rapidly  as  normal,  and 
the  conditions  for  decomposition  being  favourable,  the  taking  of 
additional  food  l)efore  the  stomach  is  ready  for  it  results  in  serious 
disturbances. 

rurthermore,  tliese  patients  are  often  tormented  by  thirst  and 
are  permitted  to  pour  down  liquids  of  all  kinds  into  the  already 
distended  and  irritated  viscus  at  irregular  intervals,  so  that  ab- 
dominal distention,  eructations,  flatulence,  and  increased  dysp- 
ncea  add  to  the  patient's  distress.  These  considerations  have  in- 
duced me  to  set  five  or  five  and  a  half  hours  as  the  proper  length 
of  the  interval  that  should  elapse  between  the  meals.  I  do  not 
])C'rmit  milk  to  be  taken  between  times,  since  by  being  curdled  in 


THE   TREATMENT   OP  VALVULAR   HEART-DISEASE  473 

the  stomach  it  is  practically  the  same  as  solid  food.  When  in 
some  cases  the  feeling  of  faintness  and  weakness  makes  some 
intermediate  nourishment  unavoidahlc;  I  order  a  clear  broth  or 
bouillon,  or  weak  tea  containing  a  little  cream  but  no  sugar,  etc. 
So  simple  a  restriction  as  this  has  often  been  found  to  work  won- 
ders in  removing  the  thirst  and  epigastric  gnawing.  A  cupful  of 
hot  water  drunk  an  hour  previous  to  a  meal  seems  to  facilitate 
the  expulsion  of  the  stomach  contents  and  to  clear  the  way  for  the 
ingestion  of  fresh  food. 

The  next  rule  is  the  restriction  of  the  quantity  of  fluids  to  be 
taken  with  meals.  In  severe  cases  liquids  should  be  limited  to  6 
ounces,  and  even  in  mild  ones  10  ounces  should  be  the  maximum. 
This  does  not  mean  only  water  in  addition  to  any  other  fluids 
that  may  have  been  ordered,  but  includes  all  liquids  combined 
and  consumed  in  addition  to  solid  ingesta.  The  purpose  of  this 
restriction  is  to  prevent  undue  distention  of  the  stomach  in  those 
cases  in  which  such  distention  would  be  likely  to  occasion  short- 
ness of  breath  or  embarrassed  cardiac  action. 

The  rule  is  that  patients  are  to  be  restricted  in  the  amount  of 
their  solid  food,  for  it  is  not  rarely  observed  that  they  manifest  a 
veritable  bulimia,  and  if  permitted  to  do  so  will  overload  their 
stomach  and  sorely  overtax  their  digestive  and  assimilative  capa- 
city. A  simple  and  usually  sufficient  guide  as  to  the  amount  that 
may  be  safely  consumed  is  to  be  found  in  the  injunction  that  they 
finish  each  meal  feeling  they  could  eat  more.  A  little,  well 
digested,  is  worth  far  more  than  a  good  deal,  poorly  digested. 
This  restriction  not  only  lessens  the  danger  of  distending  the 
atonic  organs  which  it  has  been  shown  furthers  decomposition, 
but  it  tends  to  prevent  the  cardiac  embarrassment  occasioned  by 
repletion.  Such  a  limitation  of  the  patient's  food  must  not  be 
carried  to  the  extent  of  starvation ;  and  yet  if  the  quality  of  the 
nourishment  is  judiciously  selected  it  will  often  be  a  matter  for 
surprise  how  small  a  bulk  will  suffice — nay,  how  it  will  minister 
to  the  patient's  comfort. 

In  considering  the  articles  of  food  suitable  to  this  class  of  suf- 
ferers I  think  it  best  to  deal  with  the  subject  in  a  general  way 
rather  than  to  attempt  to  make  up  appropriate  menus.  Tea  and 
coffee  should  be  weak  and  contain  such  an  amount  of  sugar  and 
cream  as  depends  upon  the  degree  of  digestive  disturbance.  Cocoa 
33 


474  •  DISEASES  OP  TEE   HEART 

or  Lroiiia  is  preferable  to  clioeolate  because  containing  less  fat, 
and  when  made  with  milk  is  nutritious.  If  wine  or  liquor  is 
thought  advisable,  it  should  be  freely  diluted  with  water.  But- 
termilk, kumjss,  and  malted  milk  make  a  valuable  addition  to  the 
dietary,  and  generally  agree  well. 

Effervescing  beverages  are  objectionable  on  account  of  the 
distention  they  occasion ;  and  for  this  and  other  reasons  malt  bev- 
erages are  not  advisable,  unless  in  special  cases  when  they  are 
craved  on  account  of  their  bitter  taste  or  their  stimulating  the 
flagging  appetite.  Iced  drinks  and  very  hot  fluids  are  not  well 
borne,  since  medium  temperatures  are  better  for  weak  stomachs. 
The  admissibility  of  soups  and  l)roths  must  be  determined  by  the 
condition  of  the  kidneys  and  the  habits  of  the  individual.  When 
chronic  ne])hritis  exists,  stock  soups  and  meat  extracts  are  to  be 
forbidden,  since  animal  extractives  are  irritating  to  the  renal 
epithelium.  It  should  be  remembered  that  beef-tea  and  the  like 
are  stimulants  and  possess  no  real  food  value.  Cream  soups,  or 
purees  as  they  are  called,  are  not  open  to  the  same  objection  and 
are  highly  nutritious.  All  these  are  fluids,  however,  and  when 
taken  in  connection  with  solid  food  should  be  limited  in  amount, 
lest  they  blunt  the  appetite  for  what  is  to  follow  and  create  a 
feeling  of  repletion. 

Carbohydrates  should  be  allowed  but  sparingly  because  of  the 
following  considerations:  In  the  first  place  they  readily  undergo 
fermentation  and  occasion  flatulent  distention  of  the  stomach  and 
bowels;  while  in  the  second  place  they  are  so  readily  oxidized  that 
they  appropriate  the  oxygen  necessary  for  the  utilization  of  the 
nitrogenous  principles  of  the  dietary. 

Nevertheless,  sugars  and  starches  cannot  be  withheld  entirely, 
and  hence  they  must  be  in  the  least  objectionable  forms.  To 
diminish  their  tendency  to  fermentation  the  latter  should  be  so 
thoroughly  subjected  to  heat  in  cooking  that  the  starch  granules 
become  converted  into  grape-sugar.  Toast,  zwieback,  light  crack- 
ers, and  "  pulled  bread  "  and  muffins  or  tea  biscuits  made  with 
baking-powder  are  preferable  to  bread  which  has  been  raised  by 
means  of  yeast  and  is  often  imperfectly  baked.  If  potatoes  are 
allowed,  they  should  l)e  baked  and  mealy,  and  even  cooked  in  this 
way  they  should  not  be  taken  in  unlimited  amounts.  Rice  when 
well  boiled  may  be  also  permitted  in  restricted  quantity,  but  sweet 


THE  TREATMENT   OF   VALVULAR   HEART-DISEASE  475 

potatoes,  cereals,  and  tlie  multifarious  combinations  of  flour,  but- 
ter, and  sugar,  whether  with  or  without  eggs  and  milk,  known  as 
cake,  griddle-cakes,  etc.,  are  inadmissible. 

Most  desserts,  and  in  particular  sweetmeats,  confections,  pre- 
served and  canned  fruits,  are  to  be  allowed  only  to  those  patients 
who  can  dispose  of  such  articles  without  annoying  flatulence. 
Fruits  are  best  in  their  natural  state,  and  even  then  should  be  ripe 
and  fresh.  Apples  are  particularly  good  because  of  their  rela- 
tively large  percentage  of  nucleo-albumin,  and  when  baked  are 
often  better  tolerated  than  when  uncooked.  Pineapple  has  always 
seemed  to  me  a  particularly  desirable  fruit  because  containing 
a  natural  digestive  ferment  of  great  efficiency.  As  a  general 
thing  I  regard  it  as  better  for  cardiopaths  to  take  fruits  at  the 
close  rather  than  at  the  beginning  of  a  meal,  as  they  do  not  blunt 
the  appetite  nor  create  so  much  gas. 

Most  of  the  fresh  vegetables  are  valuable  additions  to  the 
dietary,  either  because  rich  in  proteids  and  other  nutritive  prin- 
ciples, or  on  account  of  their  serving  as  relishes  and  containing 
various  salts  essential  to  the  organism.  Peas,  lentils,  string- 
beans,  and  spinach  are  said  to  be  relatively  rich  in  iron-forming 
principles.  Tomatoes,  cabbage,  cauliflower,  turnips,  and  kindred 
varieties  are  apt  to  disagree,  but  if  well  borne  may  be  permitted. 
Asparagus,  when  not  contra-indicated  by  renal  disease,  celery,  let- 
tuce, greens  of  various  kinds,  and  young  onions  are  allowable, 
while  cucumbers,  tender  radishes,  and  olives  may  be  left  to  indi- 
vidual desire  and  ability  to  tolerate  without  distress.  Mush- 
rooms are  very  rich  in  proteids,  and  for  renal  patients  supply  a 
form  of  nitrogenous  food  that  is  not  open  to  objection  as  is  animal 
food  with  its  extractives.  Beets  are  rich  in  sugar,  as  is  corn,  and 
are  likely  to  occasion  flatulence. 

Of  foods  rich  in  proteids  beef  and  pork  head  the  list,  but 
perhaps  are  not  so  easily  digested  as  are  veal,  lamb,  and  mutton, 
which  are  excellent  when  not  too  fat.  All  meats  should  be  roasted, 
broiled,  or  stewed,  not  fried ;  but  however  prepared,  they  should 
be  as  free  from  gravy  as  possible  and  ought  to  be  so  well  done  as 
to  have  destroyed  the  germs  of  decomposition  through  whose 
action  during  the  time  of  hanging  the  meat  becomes  tender.  Fowl 
and  game-birds  form  a  capital  adjunct  to  the  heavier  meats,  as  also 
do  fish  and  most  kinds  of  shell-fish,  particularly  oysters  when  raw. 


476  DISEASES   OF   THE   HEART 

Some  of  the  salted  fish  and  meats  when  n.ot  too  rich  provide  appe- 
tizing and  nutritions  dishes.  Canned  sahnon,  sausages,  etc.,  are 
too  rich  in  oil  and  fat,  and  are  apt  to  cause  eructations,  whereas 
fresh  tripe  is  said  to  be  easy  of  digestion.  Cheese  is  highly  nutri- 
tious, and  when  known  not  to  occasion  constipation  or  distress 
may  be  allowed.  This  is  especially  the  case  with  cottage  and 
cream  cheese.  This  article  of  food  should  not  be  taken  when 
cooked.  Eggs  are  very  digestible  and  form  a  valuable  addition  to 
the  dietary  of  this  class  of  invalids. 

Years  of  experience  in  the  feeding  of  cardiopaths  has  con- 
vinced me  that  their  food  should  be  plain  and  that  where  more 
than  ordinary  indigestion  exists  the  menu  should  not  be  elaborate. 
It  has  seemed  to  me  an  excellent  plan  in  some  instances  to  sepa- 
rate the  carbohydrates  from  the  aninuil  foods — that  is,  to  give 
them  by  themselves.  Then  at  the  meals  composed  chiefly  of  ani- 
mal food  only  vegetables  or  relishes,  such  as  asparagus,  lettuce,  or 
celery,  are  allowed  in  addition.  In  this  manner  has  been  pre- 
vented much  of  the  putrefactive  decomposition  of  meats  which 
engender  the  distressing  symptoms  of  indicanuria  and  oxaluria. 

In  conclusion,  a  few  words  may  not  be  amiss  concerning  an 
absolute  milk  diet  in  cases  of  cardiac  inadequacy.  It  has  been 
highly  recommended  in  conjunction  with  absolute  physical  rest  as 
an  excellent  means  of  restoring  compensation  when  this  is  threat- 
ened. It  acts  probably  by  lowering  arterial  tension  and  lessening 
or  removing  the  evils  of  the  defective  digestion  of  solid  food,  since 
milk  alone  acts  as  an  intestinal  antiseptic.  Furthermore,  by 
virtue  of  its  sugar,  milk  often  exerts  a  pronounced  diuretic  action, 
and  thus  aids  in  the  removal  of  minor  degrees  of  dropsy.  When 
administered  as  the  exclusive  article  of  diet,  it  is  best  given  blood- 
warm  and  in  moderate  amounts  at  regular  intervals — e.  g.,  a 
cuj)ful  every  two  hours.  It  sometimes  agrees  best  when  diluted 
with  an  alkaline  water,  as  Vichy  or  Seltzer  water.  Such  a  diet 
should  not  be  maintained  indefinitely,  and  in  most  instances  pa- 
tients begin  to  plead  for  more  substantial  nourishment  at  the  end 
of  two  or  three  days.  It  should  be  ])ersisted  in,  however,  until 
the  results  aimed  at  liave  Ijocu  readuMl,  when  a  gradual  return  to 
solid   food   is  to  be  iikhIc. 

Clothing,  Habits,  Occupation. — What  has  been  said  in  preced- 
ing pages  under  these  heads  applies  with  still  greater  force  to 


THE   TREATMENT   OP  VALVULAR  HEART-DISEASE  477 

subjects  of  valvular  niiscliief  Avlicn  their  compensation  is  imper- 
fect. The  influence  of  these  factors  is  subsidiary  to  those  that 
have  just  been  considered,  and  yet  these  matters  are  by  no  means 
unimportant.  A  too  tight  corset  or  waistcoat  may  so  hamper 
thoracic  movements  and  so  impinge  on  the  distended  right  or  left 
ventricle  as  to  frustrate  all  attempts  to  reinstate  compensation  by 
digitalis,  resistance  exercises,  baths,  etc.  Constriction  of  the 
chest  and  abdomen  is  therefore  to  be  sedulously  guarded  against. 

The  immoderate  use  of  tobacco  will  assuredly  prove  depress- 
ing to  the  heart-walls  we  are  striving  to  strengthen.  Alcoholic 
excess,  even  though  intoxication  does  not  result,  injures  an  un- 
compensated heart  by  causing  excitation  and  exhaustion  of  the 
cardiac  muscle-fibres.  Sexual  excess,  perhaps  even  very  moderate 
indulgence  of  this  kind,  may  maintain  or  increase  the  very  dila- 
tation we  are  endeavouring  to  overcome.  It  should  therefore  be 
strictly  forbidden  until  such  time  as  the  heart-power  shall  have 
been  reinstated. 

Occupation  of  all  kinds,  particularly  such  as  involve  even  the 
lightest  possible  physical  effort,  and  exciting,  long-continued  brain 
work,  must  be  laid  aside  while  compensation  is  defective.  Unfor- 
tunately, the  circumstances  of  the  patient  do  not  always  admit  of 
a  rigid  enforcement  of  this  injunction.  When  this  is  the  case, 
the  danger  of  injury  from  his  occupation  must  be  explicitly 
stated,  that  the  work  may  be  performed  in  the  easiest  possible 
manner.  It  is  always  w^ell  to  furnish  such  explanation,  together 
with  a  warning,  that  in  the  event  of  damage  resulting  from  a  con- 
tinuance of  the  employment  the  physician  may  not  be  held  respon- 
sible for  the  failure  of  treatment.  Only  by  attention  to  details 
can  the  medical  man  hope  to  turn  what  threatens  to  prove  a  disas- 
trous defeat  into  a  brilliant  and  it  may  even  be  an  unexpected 
victory.  It  is  precisely  in  this  class  of  cases  that  modern  cardio- 
therapy  obtains  its  most  signal  and  astonishing  triumphs.  There 
is  no  other  class  of  cases  which  so  amply  rewards  intelligent  and 
painstaking  management. 


CHAPTER    XVIII 

THE    TREATMENT    OF    VALVULAR    HEART-DISEASE 

{Concluded) 

III.    COMPENSATION  LOST 

In  some  cases  of  valvular  disease  that  have  reached  this  stage, 
restoration  of  their  compensation  is  impossible  and  the  physician 
can  do  no  more  than  mitigate  the  jDatient's  suiferings  or  add  a  few 
weeks  or  months  to  his  life.  In  other  cases  skilful  management 
may  so  assist  the  heart  in  its  struggle  that  it  is  able  to  overcome 
the  obstacles  in  the  way  of  the  circulation  and  regain  a  measure 
of  its  former  adequacy.  The  weapons  with  which  to  aid  Nature 
are  at  the  command  of  all,  but  the  knowledge  how  to  make  them 
most  effective  is  possessed  by  only  a  few.  Digitalis  is  the  weapon 
on  which  chief  reliance  is  to  be  placed.  It  has  its  congeners,  which 
are  sometimes  of  greater  service  because  of  some  differences  in 
their  action — e.  g.,  strophanthus,  which  exerts  less  constricting 
effect  on  the  arterioles.  It  is  safe  to  say,  however,  that  thera- 
peutists of  greatest  experience  place  more  reliance  on  digitalis 
than  any  other  remedy  of  its  class,  and  that  as  a  clinician  grows 
in  experience  in  the  treatment  of  this  group  of  lesions  he  generally 
comes  to  employ  this  drug  more  and  more  often,  and  strophanthus 
and  similar  remedies  with  decreasing  fre(pieney. 

It  is  not  alone  necessary  to  have  knowledge  of  its  mode  of 
action;  one  must  also  understand  the  indications  and  contra-in- 
dications  for  its  use.  The  skilled  hunter  will  procure  more  game 
with  an  expenditure  of  less  ammunition  than  will  an  untrained 
sportsman.  So  likewise  with  this  great  remedy.  The  experi- 
en('('(l  and  skilled  clinician  will  acconijilish  more  oftentimes  with 
small  doses  than  can  he  who  is  not  trained  to  recognise  the  condi- 
ti(ms  that  do  or  do  not  call  for  its  administration.  Inexperienced 
])ractitioners  are  apt  to  think  they  must  order  digitalis  so  soon  as 
called  on  to  treat  a  case  of  valvular  disease  willj  ruj)tured  cora- 
478 


THE  TREATMENT  OF   VALVULAR  HEART-DISEASE         479 

pensation,  no  matter  how  great  the  visceral  congestion  or  extensive 
the  (Edema.  Indeed,  the  presence  of  dropgy  is  generally  consid- 
ered the  indication  for  digitalis,  and  hence  this  drug  is  prescribed 
as  the  sovereign  remedy ;  when  this  fails,  the  case  is  considered 
hopeless.  As  a  general  proposition  it  is  true;  bnt  in  many  cases 
the  giving  of  digitalis  at  first  is  analogous  to  whipping  a  horse 
that  cannot  draw  his  load  up  hill.  He  fails,  not  because  of  lack 
of  effort,  but  because  his  load  is  beyond  his  strength.  Lighten  his 
load,  and  the  poor  beast  will  surmount  the  hill  without  faltering. 
The  crippled  heart  fails  in  its  labours,  as  a  rule,  because  its  task 
has  become  too  great,  and  not  from  weakness  inherent  in  its  myo- 
cardium. It  has  become  like  a  jaded  horse,  exhausted  yet  willing 
still,  which  may  respond  for  a  time  to  whip  and  spur,  but  will 
die  in  the  attempt. 

Overdilatation — that  is,  overdistention — of  the  cardiac  cavities 
renders  the  heart  incapable  of  responding  to  a  drug  which  slows 
the  organ  by  prolonging  diastole  and  thus  favouring  a  better  fill- 
ing of  its  chambers.  The  heart  is  already  filled  to  its  utmost  and 
fails  to  contract  adequately  because  of  abnormal  endocardial 
blood-pressure.  Even  under  the  stimulus  of  digitalis  its  walls 
cannot  cope  successfully  with  its  contents.  As  a  matter  of  fact, 
the  drug  only  intensifies  its  embarrassment.  The  stasis  within  the 
organ  must  first  he  relieved,  after  which  digitalis  may  he  adminis- 
tered with  satisfactory  results.  This  may  be  done  by  bloodletting 
or  by  catharsis;  12  to  16  ounces  of  blood  may  be  drawn  from  the 
arm,  or  wet  cups  or  leeches  may  be  applied  to  the  pracordia.  I 
prefer,  and  have  usually  employed,  hydragogue  cathartics,  because 
they  lessen  directly  the  hepatic  stasis  that  coexists  with  the  cardiac 
distention  and  forms  another  of  the  conditions  acting  as  a  barrier 
to  the  action  of  digitalis.     The  following  is  a  case  in  point : 

April  17,  1895,  I  was  asked  to  treat  Miss  T.,  aged  forty-four, 
who  had  been  ill  with  heart-disease  for  about  six  weeks  and  had 
been  given  up  by  a  number  of  doctors  as  a  hopeless  case.  In  fact, 
the  last  physician  had  declared  nothing  could  be  done  for  her, 
had  acted  on  this  belief,  prescribed  only  some  codeine  to  relieve 
her  cough,  and  had  gone  his  way.  The  lady  gave  a  history  of 
articular  rheumatism  twenty-five  years  before,  since  which  time 
she  had  been  short  of  breath.  Her  present  symptoms,  however, 
dated  from  about  six  weeks  back,  yet  could  not  be  traced  to  any 


480  DISEASES  OP  THE  HEART 

sj^ecial  exciting  cause.  A  j)roiiomice(l  aggravation  of  her  condi- 
tion had  followed  the  exertion  on  the  previous  Sunday  of  dress- 
ing and  going  downstairs  to  dinner. 

I  found  her  sitting  up  in  bed  on  account  of  dyspnoea  and  cough 
which  had  prevented  sleep  for  several  nights.  Her  colour  was 
a  peculiar  bluish-yellow  or  slightly  greenish  hue,  and  anasarca  was 
extreme,  extending  to  the  trunk,  and  including  the  upper  extremi- 
ties. The  radial  pulses  were  so  ilickering  that  the  heart-rate  had 
to  be  counted  by  auscultation.  As  nearly  as  I  could  determine, 
owing  to  the  great  arrhythmia,  the  heart  was  beating  between  160 
and  170  times  a  minute.  There  was  no  cardiac  impulse  percep- 
tible. Both  absolute  and  relative  dulness  w^as  enormously  in- 
creased, the  latter  reaching  from  1^  inch  to  the  right  of  the  right 
sternal  margin  very  nearly  to  the  left  anterior  axillary  line. 
Heart-sounds  were  feeble,  the  first  being  partly  obscured  by  a 
murmur  that  seemed  to  possess  an  indistinct  presystolic  portion ; 
the  pulmonic  sound  was  very  accentuated  and  the  corresponding 
aortic  was  weak.  The  bases  of  both  lungs,  jiarticularly  the  right, 
showed  dulness  that  did  not  shift,  and  numerous  fine  moist  rilles. 
The  firm  rounded  border  of  the  liver  was  palpable  three  finger- 
breadths  below  the  costal  arch,  and  the  abdomen  yielded  signs  of 
ascites.  The  urine  showed  nothing  more  than  the  usual  changes 
of  congestion. 

The  patient's  distress  was  pitiful,  unable  to  eat  or  sleep,  hold- 
ing herself  upright  in  bed  without  even  the  support  of  pillows, 
labouring  for  air,  coughing,  and  expectorating  bloody,  frothy 
mucus.  The  diagnosis  was  plain — mitral  disease  of  rheumatic 
origin,  which  at  last  had  broken  down  and  led  to  this  enormous 
dilatation  of  the  heart,  hypostatic  pulmonary  congestion,  hepatic 
engorgement,  tcdema,  and  ascites.  There  were  no  serious  com- 
plications, and  yet  it  Avas  very  questionable  whether  or  not  the 
heart-walls  would  ever  recover  from  the  enormous  strain  to  which 
they  were  subjected.  To  the  family  I  expressed  a  guarded  opin- 
ion as  to  the  result  of  treatment,  yet  encouraged  the  sufferer  to 
ho]»o  for  recovery,  that  she  might  siniimon  courage  from  hope  to 
endure  the  vigorous  onslanghts  on  her  (rdema  that  would  have  to 
be  made.  It  seemed  to  me  useless  to  prescribe  digitalis  with  the 
heai't  in  that  state;  so  T  resolved  to  sustain  it  with  strychnine, 
which,  owing  to  the  fact  that  she  could  not  afi'ord  a  nurse,  was 


THE  TREATMENT   OP   VALVULAR  HEART-DISEASE  481 

given  by  inoiitli,  g^^  every  three  hours  during  the  day,  while  each 
evening  I  injected  the  same  dose  hypodermically,  together  with  -J 
of  morphine  and  yj-^  of  atropine,  to  induce  sleep  and  lessen  the 
cough.  Then  as  a  package  of  symphorol  had  been  given  me  for 
trial,  I  decided  to  try  its  effect  on  the  dropsy.  A  cathartic  was 
also  administered,  but  not  a  very  powerful  one.  The  diuretic 
failed  absolutely,  and  Merck's  diuretin  was  tried  with  the  same 
want  of  success.  Then  without  changing  the  strychnine  and  even- 
ing dose  of  morphine  it  was  decided  to  make  use  of  purgation — 
good,  vigorous  purgation  of  the  old-fashioned  sort. 

The  patient's  strength,  by  the  way,  had  increased  appreciably, 
although  the  oedema  had  only  grown  somewhat  less  hard.  She 
was  also  able  to  take  a  little  more  nourishment,  consisting  of  milk 
and  eggs.  Accordingly  compound  jalap  powder  in  teaspoonful 
doses  was  administered  until  a  large  number  of  copious  watery 
stools  were  secured.  Indeed  at  one  of  my  visits — the  first,  I  be- 
lieve, after  the  powder  had  been  ordered — she  was  found  sitting 
on  the  night-stool,  and  in  response  to  my  queries  concerning  the 
effect  of  treatment,  stated  she  had  been  sitting  there  for  two  hours, 
preferring  that  to  the  effort  and  fatigue  of  changing  from  bed  to 
the  stool  and  back  again  every  few  minutes.  The  influence  on  the 
heart  and  circulation  was  wonderful  and  gratifying.  First  her 
cough  and  dyspnoea  subsided  and  the  sputum  lost  its  bloody  char- 
acter ;  the  abdomen  softened  down,  and  the  oedema  left  the  arms 
and  flanks;  the  pulse  grew  a  trifle  less  rapid,  but  appreciably 
more  waves  reached  the  wrist ;  cardiac  dulness  became  rather  less 
extensive  also.  Then  I  decided  to  let  up  a  little  on  the  purgation 
and  to  administer  infusion  of  digitalis  carefully  prepared  from 
English  leaves,  strychnine  and  morphine  to  be  continued  as  be- 
fore. The  results  were  almost  magical;  the  heart  quieted  down 
and  daily  grew  in  regularity  and  strength;  dropsy  disappeared 
entirely,  and  the  patient,  free  from  cough,  was  able  to  lie  down 
with  ease  and  enjoy  a  comfortable  night's  sleep.  The  morphine 
was  discontinued,  but  the  strychnine  was  left  undisturbed. 

May  1st  the  patient  was  turned  over  to  Dr.  Houston,  who 
resided  in  the  neighbourhood,  and  by  him  reports  of  her  progress 
were  made  to  me.  The  last  time  I  saw  the  patient,  about  June 
1st,  she  was  sitting  dressed  on  a  sofa,  without  the  faintest  trace 
of  oedema,  the  pulse  80,  perfectly  regular,  the  heart  of  nearly 


482  DISEASES  OF  THE  HEART 

normal  size,  and  witli  a  loud  systolic  apex-murmur.  Compensa- 
tion had  become  re-established  for  the  time.  A  peculiar  and  inter- 
esting feature  of  this  case  now  developed;  the  patient  became 
quiet,  morose,  and  melancholy,  very  unlike  her  cheerful,  patient 
self  during  the  height  of  her  peril.  This  change  of  disposition  Dr. 
Houston  found  was  due  to  digitalis  and  disappeared  with  cessa- 
tion of  the  drug.  This  patient  removed  during  that  same  summer 
to  Moline,  and  there,  her  old  symptoms  of  asystolism  returning, 
she  died  in  February,  1896. 

In  this  case  the  treatment,  though  successful,  was  severe,  and 
under  similar  conditions  I  would  now  advise  removing  the  ascites 
by  aspiration,  which,  by  more  quickly  relieving  intra-abdominal 
pressure,  would  permit  the  earlier  employment  of  digitalis.  In 
most  cases  of  the  kind,  moreover,  diuretin  accomplishes  the  re- 
moval of  the  dropsy.  Its  failure  in  this  instance  was  owing  prob- 
ably to  the  extreme  renal  stasis,  which  should  first  have  been 
lessened.  I  have  seen  remarkable  results  follow  its  use  in  cases 
of  cardiac  dropsy  in  which  stasis  was  less  pronounced. 

A.  C,  a  tall,  slender  girl  of  fourteen  years,  was  seen  in  con- 
sultation with  the  late  Dr.  E.  M.  Hale,  December  14,  1891,  be- 
cause of  heart-disease  and  increasing  dropsy.  There  was  a  his- 
tory of  chorea  at  eight  years  of  age  and  again  in  August,  1891, 
since  which  latter  attack  she  had  not  been  well.  Oedema  had 
gradually  appeared  and  increased  in  spite  of  treatment  by  her 
home  physician ;  hence  she  had  been  brought  to  Chicago  and 
jjlaced  in  charge  of  Dr.  Hale.  A  urine  analysis  of  December  9th 
by  Dr.  C.  Mitchell  had  shown  a  fourteen-hour  quantity  of  13 
ounces,  specific  gravity  1.027,  acid,  urea  stated  as  reduced  to  75 
per  cent  of  normal,  a  small  amount  of  albumin  and  hyaline  and 
granular  casts.  The  symptoms  were  the  usual  ones  of  dyspncca, 
weakness,  and  swelling  of  the  lower  extremities,  anorexia,  and 
constipation. 

The  patient  lay  on  a  couch  semi-recumbent,  evincing  plain 
signs  of  venous  stasis.  The  lower  extremities  were  moderately 
ocdematous,  and  the  external  jugulars  were  distended,  but  not 
]))ilsating.  There  was  noticeable  prominence  of  the  prjTCordium 
and  great  distention  of  the  abdomen,  which  yielded  signs  of  free 
fluid,  the  liver  being  palpable  three  finger-breadths  below  the  cos- 
tal arch.     The  heart  was  greatly  increased  in  size,  the  apex-beat 


THE  TREATMENT  OP  VALVULAR  HEART-DISEASE         483 

being  in  the  sixth  left  interspace  outside  the  nipple,  and  there  was 
a  loud  mitral  systolic  and  short  presystolic  murmur.  My  notes  do 
not  state  the  pulse-rate,  but  mention  that  the  pulse  was  regular, 
rapid,  and  small.  Signs  of  the  heart  being  immovably  fixed  in 
position  were  discovered  at  a  much  later  period. 

In  view  of  the  fact  that  die-italis  had  been  taken  without 
favourably  influencing  the  dropsy,  it  was  decided  to  put  her  on 
90  grains  of  diuretin  in  twenty-four  hours  and  administer  a 
moderate  dose  of  calomel.  Two  days  subsequently  the  urine  was 
reported  to  be  81  ounces  and  to  contain  a  trace  of  albumin  but 
no  casts.  This  wilful  little  miss  then  began  to  be  so  annoyed  by 
the  frequent  micturition  that  she  refused  any  longer  to  take 
diuretin,  and  this  was  stopped.  It  was  replaced  by  heart-tonics, 
first  digitalis,  and  then  -^  grain  of  convallamarin  thrice  daily. 
Her  improvement  was  so  rapid  that  after  about  two  weeks  she  was 
taken  to  her  Iowa  home  in  care  of  a  trained  nurse,  by  whom  orders 
as  to  diet  and  exercise  were  strictly  enforced.  Uninterrupted 
gain  was  made  until  February,  when  the  patient  wearied  of  her 
restraint  and  my  services  were  dispensed  with.  The  following 
October  I  learned  that  she  was  riding  horseback,  playing  lawn- 
tennis,  and  bicycling,  but  ''  her  lips  looked  blue."  Five  years  now 
elapsed  before  I  again  saw"  her,  but  I  learned  meanwhile  that  she 
had  another  breakdown  similar  to  her  first  one,  her  recovery  being 
very  slow,  and  requiring  severe  purgation. 

My  next  examination  of  this  patient  was  in  the  early  fall  of 
1896,  at  which  time  she  was  attending  a  young  ladies'  school  in 
one  of  our  suburbs.  The  heart  was  very  greatly  enlarged;  its 
apex-beat  was  immovable  in  the  sixth  left  interspace  well  towards 
the  anterior  axillary  line;  and  mitral  regurgitation  appeared  to 
be  the  predominant  lesion.  Hepatic  engorgement  was  consider- 
able and  cardiac  embarrassment  was  evident  upon  exertion.  She 
was  resorting  occasionally  to  a  few  drops  of  strophanthus,  but  no 
cathartics. 

She  was  induced  to  take  a  laxative  water  at  regular  intervals, 
which  speedily  lessened  the  visceral  congestion.  She  also  con- 
sented to  try  the  efficacy  of  a  course  of  baths  a  la  Nauheim  sup- 
plemented by  resistance  gymnastics.  The  results  were  gratifying, 
the  dilatation  of  the  right  heart  being  appreciably  reduced  and 
the  cardiac  tone  in  general  being  greatly  improved  for  the  next 


484  DISEASES  OP   THE   HEART 

two  years,  as  she  subsequently  stated.  She  passed  the  winter  of 
lS98-'i)9  at  a  young  ladies'  school  near  Philadelphia,  and  was  in 
tolerable  health  until  April,  1899,  when  she  had  an  attack  of 
acute  rheumatism.  This  resulted  in  an  acute  pericarditis  with 
effusion,  which  left  her  very  feeble  for  the  ensuing  two  months, 
much  of  that  time  being  spent  in  a  wheel-chair  at  Atlantic  City. 
I  had  the  opportunity  of  examining  her  in  June,  when  the  heart 
was  found  enormously  enlarged,  with  an  intense  systolic  apex-mur- 
mur, and  also  a  loud  diastolic  one  immediately  following  the  sec- 
ond sound.  This  murmur  was  of  nuiximum  intensity  at  and  about 
the  apex,  and  was  evidently  mitral^  produced  by  the  inrush  of 
blood  into  the  dilated  left  ventricle  during  the  beginning  of  its 
diastole.  The  action  of  the  heart  was  unsteady,  the  abdominal 
organs  were  much  engorged,  and  the  patient  was  pale  and  weak. 
She  was  put  on  strophanthus,  strychnine,  and  iron,  and  went  on 
to  her  home.  Her  condition  improved  during  that  summer,  yet 
remembering  the  benefit  obtained  by  the  Nauheim  treatment  in 
1896,  she  returned  for  another  course  in  October,  1899. 

My  notes  record  that  the  apex-impulse  was  broad  and  heaving 
in  the  sixth  and  seventh  interspaces  5  inches  to  left  of  the  ster- 
num ;  absolute  and  relative  dulness  greatly  increased,  the  latter  ex- 
tending nearly  to  the  left  anterior  axillary  line,  and  at  the  right 
to  1^  inch  to  the  right  of  the  breastbone.  The  apex  was  fixed  in 
position,  and  a  double  murmur  was  still  present  in  the  mitral 
area,  both  very  intense.  The  external  jugulars  were  full  and 
the  liver  palpable.  Signs  of  insufficiency  of  the  aortic  valves  were 
diligently  sought  for,  but  in  vain.  The  mitral  valves  alone  were 
involved.  The  enormous  hypertrophy  and  dilatation  of  the  left 
ventricle  were  due  to  the  exo-pericardial  adhesions  acting  in  con- 
junction with  the  mitral  disease.  Baths  and  exercises  w^ere  begun 
()(!tober  19tli,  and  j^ovember  1st  it  was  recorded  that  the  left 
external  juguhir  was  turgid.  The  ])ati('nt,  conlrarv  to  instruc- 
tions, was  ascending  too  many  stairs  and  eating  too  heavily.  Ca- 
tharsis and  great  care  in  the  matter  of  exercising  reduced  the 
turgescence  of  the  veins  and  liver  for  a  while.  On  November 
2'>d  it  was  again  recorded  that  the  jugulars  were  full  and  the  lips 
blue.  This  was  attributed  to  her  having  hurried  in  dressing 
and  having  walked  against  a  strong  cold  wind.  The  venous  con- 
gestion again  dimiiiislicd,  althoiigli   iml   entirely.      At  the  close  of 


THE  TREATMENT   OP  -VALVULAR   HEART-DISEASE  485 

the  course  of  treatments,  which  had  extended  throngh  six  weeks, 
it  was  noted  that  the  left  heart  had  not  diminished  in  size  at  alL 
The  enlargement  of  the  right  heart  was  less,  however,  the  action 
of  the  heart  less  easily  disturbed,  and  the  patient  felt  stronger, 
having  lost  the  weakness,  perspirations,  and  sensation  as  if  the 
"  heart  was  trembling,"  symptoms  of  which  she  spoke  at  the  date 
of  commencing  the  treatment.  The  winter  following  she  felt 
better  than  ever  before. 

Since  the  above  was  written  this  patient  suffered  a  final  break- 
down, and  died  under  niy  care  in  May,  1901.  Her  last  symptoms 
have  been  described  in  the  chapter  on  Mitral  Regurgitation. 

March  18,  1896,  I  was  requested  to  see  Mrs.  T.,  aged  thirty- 
four  years,  who  had  been  dropsical  for  several  months.  The 
patient  had  had  inflammatory  rheumatism  at  the  age  of  twelve  or 
thirteen  and  again  at  thirty,  soon  after  the  birth  of  her  second 
child,  but  had  not  been  aware  of  cardiac  symptoms  until  Septem- 
ber 10,  1895.  She  had  then  been  aroused  in  the  night  by  a  violent 
attack  of  palpitation ;  and  a  few  weeks  subsequently  had  suddenly 
developed  headache,  paralysis  of  the  right  side  of  the  face,  and 
partial  left  hemiplegia.  This  had  gradually  improved,  leaving 
behind  a  paralysis  of  the  extensors  of  the  left  arm  and  contracture 
of  the  fourth  and  fifth  fingers.  After  this  attack  dropsy  had 
gradually  come  on,  and  had  resisted  treatment  by  several  local 
homceopathic  physicians.  For  six  weeks  prior  to  my  seeing  her 
she  had  been  unable  to  lie  down,  and  had  only  slept  by  sitting 
with  her  arms  supported  on  a  table  in  front  of  her.  An  enormous 
cedema  extended  as  high  as  the  waist  and  involved  also  the  left  or 
paralyzed  arm.  The  greatly  distended  abdomen  yielded  fiuctua- 
tion  and  percussion  evidence  of  free  fluid.  The  liver  was  made 
out  as  greatly  enlarged,  and  there  were  signs  also  of  fluid  in  the 
right  pleural  cavity.  The  pulse  in  the  right  radial  was  very 
arrhythmic,  small,  and  accelerated ;  the  left  radial  pulse  was,  and 
it  may  be  remarked  still  is,  smaller  and  feebler  than  the  right.  The 
external  jugulars  were  a  good  deal  distended  but  did  not  pulsate. 
The  apex-beat  was  in  the  seventh  and  eighth  intercostal  spaces 
close  to  the  left  anterior  axillary  line.  It  was  at  first  thought  to 
be  pushed  over  by  the  right-sided  hydrothorax,  as  the  fluid  in  the 
pleural  cavity  was  thought  to  be.  The  first  heart-sound  was  audi- 
ble in  spite  of  a  loud  systolic  murmur  which  was  transmitted 


486  DISEASES  OF  THE   HEART 

around  to  the  back;  the  puhnonic  second  sound  was  much  inten- 
sified. With  exception  of  the  shifting  dulness  at  the  right  base, 
the  lungs  Avere  negative.  The  urine  was  scanty,  but  gave  no 
evidence  of  renal  disease  apart  from  congestion. 

Tliis  case  was  thought  to  be  merely  one  of  mitral  regurgita- 
tion in  the  stage  of  destroyed  compensation.  A  year  later,  how- 
ever, well-marked  retraction  of  the  tenth  and  eleventh  left  inter- 
costal spaces  posteriorly  was  discovered,  Broadbent's  sign  of  ad- 
herent pericardium,  and  the  apex  was  immovable.  Early  in 
April,  after  I  took  charge  of  the  case,  a  quart  of  clear  serum 
was  withdrawn  from  the  right  pleural  cavity,  after  which  reso- 
nance and  vesicular  respiration  returned  to  that  side.  This  was 
after  treatment  had  removed  the  dropsy,  and  hence  this  was 
concluded  to  be  an  old  pleuritic  effusion  that  had  escaped  previ- 
ous recognition. 

The  preliminary  treatment  in  this  case,  as  in  that  of  Miss  T., 
was  heroic  purgation.  It  seemed  useless  to  administer  digitalis 
or  diuretics  until  after  the  excessive  stasis  had  been  reduced  by 
catharsis,  and  hence  the  patient  was  assured  of  relief  if  she  would 
have  the  courage  to  bear  some  very  severe  treatment.  Her  re- 
sponse was  to  the  effect  that  she  would  gladly  endure  anything 
that  would  relieve  her  of  her  suffering.  Accordingly  -^-^  of  a  grain 
of  elaterin  was  prescribed  hourly  until  it  began  to  oi)erate.  At 
my  visit  next  day  I  learned  she  had  taken  ten  of  the  elaterin 
granules  and  that  she  had  vomited  11  times  and  purged  20.  In- 
dications of  improvement  were  already  appreciable,  and  as  she 
expressed  herself  as  ready  to  stand  another  round,  the  granules 
were  ordered  repeated  on  the  following  day.  Their  effect  was 
immense,  after  which  the  dropsy  diminished  still  more.  To  sus- 
tain her  during  this  ordeal  she  received  full  doses  of  strychnine 
by  mouth,  stimulants  whenever  necessary,  and  a  concentrated 
nourishing  diet  consisting  largely  of  eggs  and  strong  broths.  By 
the  fifth  day  the  circiihition  had  manifestly  improved,  but  she 
felt  and  appeared  very  weak.  The  family  was  much  concerned 
and  thought  the  ])atient  was  never  going  to  endure  the  treatment. 
'J'he  sufferer  was  uiidininted,  however,  and  I  was  obliged  on  more 
than  one  occasion  to  censure  certain  members  of  the  family  se- 
verely for  talking  before  the  patient  in  a  way  to  dishearten  her. 
Digitalis  was  then  ordered  in  tablespoonful  doses  of  the  fresh  in- 


THE   TREATMENT   OF  .VALVULAR   HEART-DISEASE  487 

fusion  every  four  hours,  and  the  vigour  of  the  catharsis  was 
abated,  from  4  to  6  watery  stools  daily  being  still  secured.  It 
was  not  long-  before  the  patient  was  able  to  rest  in  bed,  a  thing 
she  had  not  been  able  to  do  for  nearly  two  months.  The  sceptics 
in  the  family  circle  were  now  convinced  and  ready  to  assist  in  any 
therapeutic  measure  proposed.  The  (Dedema  was  stubborn,  yet 
wholly  subsided  in  about  three  weeks.  When  this  had  been  ac- 
complished aspiration  of  the  right  pleural  cavity  was  performed 
with  the  result  previously  stated.  Digitalis  was  continued  daily 
for  a  year,  but  in  the  form  of  the  tincture  and  for  the  most  part 
in  doses  of  15  drops  three  to  four  times  a  day.  The  change  in 
the  pulse  was  very  gratifying,  being  in  June,  as  given  in  my 
notes,  only  65  and  tolerably  regular.  The  liver  still  remained 
greatly  enlarged  and  kept  showing  such  a  tendency  to  increase  in 
size  and  firmness  whenever  the  bowels  were  not  kept  freely  open 
that  at  length  the  patient  was  instructed  to  keep  on  hand  a  satu- 
rated solution  of  Epsom  salts,  and  of  this  to  take  every  morning 
such  an  amount  as  would  secure  several  fluid  evacuations.  This 
order  was  strictly  obeyed,  and  in  conjunction  with  the  cardiac 
tonics  produced  the  happiest  results.  Before  the  summer  was 
past  she  was  walking  about  the  house  and  enjoying  drives.  As- 
cending stairs  was  strictly  forbidden,  however,  and  was  not  even 
attempted  for  at  least  a  year. 

Although  this  patient  never  lost  her  appetite  and  seldom  expe- 
rienced indigestion,  her  dietary  was  made  very  simple  and  of  a 
somewhat  restricted  quantity  that  there  might  be  no  chance  of 
her  overloading  her  stomach  to  the  detriment  of  her  still  enor- 
mously hypertrophied  and  dilated  heart.  It  consisted  in  the 
main  of  a  small  dish  of  cereal  and  cream,  a  soft-boiled  egg,  a 
little  buttered  toast,  and  a  cup  of  cereal  coffee  for  breakfast ;  for 
dinner  at  midday  a  fair-sized  piece  of  meat,  green  vegetables, 
little  or  no  potatoes,  some  bread  and  butter,  and  a  simple  plain 
dessert,  as  plain  pudding,  or  some  fresh  fruit,  water  in  limited 
quantity  being  the  beverage ;  for  the  evening  meal  she  generally 
took  a  little  cold  meat  with  bread  and  butter  and  cooked  fruit  of 
some  kind.  After  a .  considerable  time,  in  consequence  of  the  de- 
velopment of  symptoms  that  seemed  to  indicate  she  was  getting 
too  much  meat  for  the  limited  amount  of  exercise,  I  took  away 
the  animal  food  in  the  evening  and  she  confined  herself  to  her 


488  DISEASES  OF   THE   HEART 

favourite  cereal  at  this  incal.  This  patient  oheyed  instructions 
to  the  letter,  and,  owing  largely  to  this  circumstance,  gained  grad- 
ually in  endurance  and  improved  in  colour  until  at  the  end  of  two 
years  was  said  by  friends  to  no  longer  look  like  an  invalid.  For 
the  past  four  years  she  has  taken  very  little  medicine  and  has 
been  able  to  attend  to  her  household,  even  doing  considerable 
work  at  different  times.  She  has  been  allowed  to  go  upstairs, 
provided  she  does  not  hurry,  and  has  not  been  injured  thereby. 
I  have  seen  her  on  the  average  once  every  two  weeks,  yet  have 
not  always  prescribed  medicine,  contenting  myself  with  seeing 
that  everything  was  progressing  as  well  as  could  be  expected. 
There  has  been  verj'  little  time  when  she  has  not  taken  a  little 
digitalis,  usually  a  single  daily  dose  of  5  or  10  drops,  but  now 
and  then,  when  the  heart  has  shown  a  disposition  to  greater 
arrhythmia  or  hurry,  this  amount  has  been  exceeded.  There 
have  been  periods  of  days  or  a  few  weeks  when  I  have  seen  fit 
to  order  iron  or  strychnine,  and  at  a  few  times,  chara'cterized 
by  unusual  constriction  of  the  pulse  and  scantiness  of  urine,  she 
has  been  obliged  to  resort  to  nitroglycerin,  usually  to  the  relief  of 
the  condition.  In  the  fall  of  1899  this  patient  contracted  a  bron- 
chitis which  was  attended  with  such  a  degree  of  fever  and  conges- 
tion of  the  right  lung  that  for  a  day  or  two  I  feared  she  would 
get  a  broncho-pneumonia.  It  finally  ^nelded,  however,  to  rest  in 
bed,  heroin  and  apomorphine  hydrochlorate,  the  heart  being 
sustained  by  some  extra  doses  of  strychnine  and  digitalis.  This 
patient  has  never  showni  much  dyspna\a,  but  did  for  a  number  of 
months  suffer  a  good  deal  from  fugitive  pains  in  the  left  half  of 
the  thorax  with  areas  of  intercostal  tenderness,  while  below  the 
right  scapula  and  passing  through  to  the  front  was  at  times  a 
wearing  dull  pain  that  was  only  mitigated  by  lying  down.  Her 
liver  is  still  very  large  and  growing,  as  the  months  go  on,  percep- 
tibly thinner  at  its  border  and  harder.  It  drops  down  also,  being 
readily  pushed  upward.  I  therefore  attributed  her  right-sided 
pain  to  the  pulling  of  the  heavy  liver  on  its  supports. 

As  the  reader  has  observed,  the  foregoing  cases  are  all  in- 
stances of  mitral  disease,  and  two  of  them  complicated  by  peri- 
cardial adhesions.  They  were  consequently  not  the  most  promis- 
ing, yet  responded  to  treatment  in  a  highly  gratifying  manner. 
Such  is  not  so  with  cases  of  aortic-valve  disease,  as  proved  by 


THE   TREATMENT   OP   '^ALVULAR  HEART-DISEASE  489 

the  cases  detailed  in  the  chapter  devoted  to  Aortic  Regurgitation. 
In  1894  I  had  in  charge  a  young  man  -nineteen  years  of  age 
afflicted  with  insufficiency  of  the  aortic  valves  of  rheumatic  origin. 
Compensation  was  not  badly  ruptured  to  judge  from  his  symp- 
toms. He  displayed  no  oedema  or  marked  venous  stasis,  almost 
his  only  subjective  consciousness  that  all  w^as  not  right  being 
shortness  of  breath  and  palpitation  upon  exertion.  Yet  the  heart 
was  dilated  and  the  pulse  notably  arrhythmic.  It  was  hoped 
benefit  would  result  from  a  course  of  therapeutic  baths  and  exer- 
cises. As  a  matter  of  fact  some  degree  of  strength  appeared  to 
be  imparted  to  the  heart,  for  the  impulse  became  more  defined, 
the  sounds  more  distinct,  and  his  subjective  sensations  less  pro- 
nounced. Nevertheless,  not  many  weeks  had  elapsed  after  the 
course  of  treatment  when  he  suddenly  had  an  attack  of  partial 
syncope,  on  account  of  which  he  was  confined  to  bed  and  cardiac 
tonics  were  administered.  He  did  not  improve,  and  a  few  days 
later  died  suddenly  with  manifestations  that  strongly  suggested 
embolism  of  one  of  the  main  divisions  of  the  pulmonary  artery. 
An  autopsy  was  not  obtained. 

The  Treatment  of  Dropsy. — When  this  supervenes  in  the  down- 
ward course  of  valve-lesions,  it  is  not  to  be  regarded  merely  as  an 
indication  of  cardiac  inadequacy,  but  as  evidence  of  obstruction 
to  capillary  circulation,  plus  ansemia  and  greater  permeability  of 
the  capillary  walls.  The  pressure  of  the  transuded  serum  still 
further  obstructs  capillary  flow  and  augments  cardiac  embarrass- 
ment. It  must  be  removed,  therefore,  before  the  strength  of  the 
heart  can  be  restored.  In  this  stage  of  valvular  disease  the  occur- 
rence of  dropsy  is  very  common,  and  its  removal  is  the  problem 
first  requiring  solution.  In  some  instances  this  is  easy  and  only 
necessitates  for  its  accomplishment  the  invigoration  of  cardiac 
contractions  by  putting  the  patient  at  rest  and  by  administering 
cathartics  and  digitalis. 

According  to  my  experience,  the  infusion  of  digitalis  exerts  a 
more  decided  diuretic  action  than  does  any  other  preparation  or 
any  other  remedy  excepting  diuretin.  It  should  be  freshly  pre- 
pared from  English  leaves,  as  these  are  more  reliable  than  the 
German,  which  are  said  to  contain  a  considerable  proportion  of 
stems.     The  substitution  of  a  fluid  extract  for  the  leaves  in  the 

preparation  of  the  infusion  is  never  to  be  tolerated.     The  addition 
33 


490  DISEASES  OP  THE  HEART 

of  squills  or  of  a  potassium  salt,  as  the  citrate  or  acetate,  is 
thought  by  some  to  intensify  the  diuretic  action  of  the  infusion, 
but  is  objectionable.  Squills  is  likely  to  occasion  irritation  of  the 
gastro-intestinal  tract  and  render  the  stomach  intolerant  of  the 
digitalis.  If  potash  is  used  in  conjunction  it  is  better  alone,  so 
that  either  of  the  drugs  may  be  increased,  decreased,  or  withdrawn 
without  affecting  the  other. 

To  procure  its  action  on  the  kidneys  the  infusion  should  be 
given  in  full  doses,  ^  an  ounce  every  four  hours,  and  continued 
for  several  days  or  so  long  as  it  continues  to  augment  the  flow  of 
urine.  Its  action  should  be  closely  watched,  that  the  remedy  may 
be  stopped  so  soon  as  signs  of  its  cumulative  effect  are  detected. 
These  are  slowing  of  the  heart's  contractions  to  60  or  less,  nausea, 
and  a  falling  off  in  the  amount  of  urine  after  this  has  first  been 
increased.  It  should  be  remembered  that  some  persons  become 
nauseated  by  digitalis  even  before  it  has  been  taken  long  enough  to 
produce  its  poisonous  effects.  The  most  trustworthy  indication 
that  the  drug  would  best  be  discontinued  is  found  in  the  excretion 
of  urine.  If  this  does  not  augment  after  digitalis  has  been  exhib- 
ited for  two  or  three  days,  even  though  the  pulse-rate  falls,  there 
is  nothing  to  be  gained  by  further  administration  of  the  medicine 
at  this  time.  If  persevered  in  there  is  danger  of  cumulative 
action.  Again,  if  after  having  been  increased  for  a  while  the 
urine  begins  to  diminish,  digitalis  is  beginning  to  exert  its  toxic 
effect,  and  ought  at  once  to  be  stopped.  Even  if  these  unfavour- 
able signs  do  not  appear  I  make  it  a  rule  to  withdraw  the  infu- 
sion at  the  end  of  five  days,  or  after  the  8  ounces  comprised  in  the 
pharmacopoeial  formula  have  been  exhausted.  The  drug  contin- 
ues to  be  eliminated  for  a  day  or  so  longer,  and  hence  it  is  not 
usually  necessary  to  follow  it  directly  by  any  other  similarly 
acting  agent. 

It  is  not  uncommon  for  digitalis  to  fail  to  remove  dropsy,  and 
when  such  is  the  case  it  is  well  to  try  diurctin — Knoll.  This  is 
often  surprising  in  its  action,  as  in  one  case  in  which  after  the 
failure  of  digitalis  it  increased  the  urine  from  a  pint  in  twenty- 
four  hours  to  8  quarts.  Even  this  remedy  may  fail,  but  if  it  is 
fresh  and  given  in  large  doses  of  90  to  120  grains  a  day  it  gener- 
ally proves  a  powerful  diuretic.  It  is  best  given  in  solution,  15 
grains  every  three  or  four  hours,  yet  in  conjunction  with  digitalis 


THE  TREATMENT   OP   VALVULAR  HEART-DISEASE         491 

smaller  doses  are  sometimes  efficient.  Diuretin  has  a  disagreeable 
soapy  taste,  and  after  a  time  may  occasion  nausea  and  even  vom- 
iting. It  also  loosens  the  bowels  in  some  instances.  Its  taste  and 
unpleasant  effects  may  be  counteracted  by  the  addition  to  each 
dose  of  a  drachm  or  two  of  essence  of  pepsin.  For  the  knowledge 
of  this  valuable  therapeutic  fact  I  am  indebted  to  the  wife  of  a 
former  patient  who  was  compelled  to  take  large  doses  of  diuretin 
for  a  long  time. 

I  have  tried  numerous  other  highly  vaunted  diuretic  reme- 
dies, but  none  aside  from  diuretin  has  ever  fulfilled  expectations. 
Sugar  of  milk  and  vegetable  diuretics,  as  apocynum  cannabinum 
and  squills,  have  never  yielded  satisfactory  results.  Indeed,  I  do 
not  see  how  they  can  be  expected  to  overcome  dropsy  when  this  is 
due  to  cardiac  inadequacy  and  renal  congestion.  The  indications 
are  to  relieve  stasis  and  to  stimulate  heart  action,  which  they  can- 
not do.  I  have  not  employed  calomel  as  a  diuretic  since  I  have 
dreaded  a  possible  ptyalism.  When  used  for  its  effect  on  the  kid- 
neys, it  is  in  doses  of  3  grains  several  times  daily  in  conjunction 
with  opium  to  restrain  its  action  on  the  bowels.  Administered 
in  this  manner  it  is  said  by  the  Germans  to  prove  highly  efficient 
in  cases  of  cardiac  dropsy  uncomplicated  by  renal  disease.  It 
seems  to  me,  however,  that  one  is  justified  in  resorting  to  so  pow- 
erful an  agent  only  when  all  other  means  have  failed. 

If  the  dropsy  is  so  extreme  that  serous  transudation  in  the 
abdomen  or  other  cavities  intensifies  the  patient's  distress,  it  is 
often  found  that  digitalis,  diuretin,  or  caffeine,  even  in  heroic 
doses,  fail  to  increase  the  urine.  This  is  due  to  the  impossibility 
of  securing  adequate  blood-pressure  in  the  renal  arteries.  Stasis 
in  the  renal  veins  must  first  be  lessened  if  one  is  to  induce  pro- 
nounced kidney  action.  For  this  reason  such  enormous  oedema 
must  be  diminished  or  removed  through  the  skin,  bowels,  or  by 
mechanical  means.  Profuse  sweating  is  not  advisable,  since  hot- 
air  baths  and  pilocarpine  are  too  depressing  for  heart  patients. 
We  are  restricted  consequently  to  catharsis  and  operative  pro- 
cedures. 

The  latter  include  punctures  or  incisions  of  the  skin  of  the 
ankles  to  permit  the  serum  to  drain  away.  This  is  often  an  effi- 
cient mode  of  removing  obstinate  dropsy,  but  is  likely  to  be  ob- 
jected to  by  the  patient  or  his  friends.     Great  cleanliness  is  re- 


4:92  DISEASES   OF   THE   HEART 

quired  to  prevent  inflammation  of  the  integument.  A  most  excel- 
lent means  of  securing  such  drainage,  and  one  not  open  to  the 
objection  of  possible  infection,  is  in  the  use  of  Southey's  tubes. 
These  are  tiny  silver  cannulas  which  by  aid  of  a  minute  trocar  can 
be  inserted  beneath  the  skin  of  the  ankles,  and  are  then  secured  in 
place  by  strips  of  adhesive  plaster  or  by  rubber  bands.  Hypo- 
dermic needles  can  be  used  in  the  same  manner.  The  quantity 
of  serum  that  will  trickle  away  through  these  tubes  is  astonishing. 

Dropsical  accumulation  in  the  serous  cavities  may  be  with- 
drawn by  tapping,  a  procedure  which,  if  slowly  done,  is  devoid  of 
danger  of  collapse.  It  occasions  pain,  and  patients  generally 
shrink  from  being  tai)ped  on  this  account.  They  also  often  urge 
the  additional  objection  that  it  Avill  have  to  be  repeated,  and  hence 
in  private  practice  it  is  seldom  resorted  to.  When  consent  to  this 
proceeding  can  be  secured,  the  physician  should  not  content  him- 
self merely  with  having  thus  removed  the  fluid.  It  will  quickly 
rcaccumulatc  unless  the  advantage  thus  gained  can  be  held.  Con- 
sequently the  tapping  should  be  followed  by  the  administration  of 
digitalis  or  diuretin,  or  both.  It  may  be  well  also  to  administer 
an  active  purge,  for  by  such  measures  recourse  to  aspiration  more 
than  once  may  perhaps  be  prevented.  In  the  case  of  most  private 
patients  it  will  be  found  that  they  prefer  active  catharsis.  They 
have  had  more  or  less  experience  with  purgation  in  times  past,  it 
may  be,  and  they  naturally  look  upon  it  as  less  painful  than  being 
tapped. 

Cathartics. — Whenever  it  becomes  necessary  to  remove  serous 
accunmhitions  through  the  intestinal  tract,  it  should  be  remem- 
bered that  it  can  only  be  accomplished  by  the  production  of  many 
copious  watery  discharges  daily.  It  is  not  sufficient  that  the  de- 
jections are  semifluid  and  number  two  or  three  daily;  Nature 
often  does  this  much  by  a  pouring  out  of  serum  into  the  intestinal 
canal,  in  consequence  of  which  the  patient  has  several  loose,  even 
liquid,  passages  daily.  In  spite  of  Nature's  treatment,  the  dropsy 
goes  on  increasing.  JSTature  thus  furnishes  the  indication  for 
treatment,  and  fortunately  we  are  able  to  aid  her  by  the  adminis- 
tration of  hydragogue  cathartics.  This  procedure  is  sometimes 
objected  to  on  the  ground  that  the  cardiac  suiferer  is  too  weak  to 
endure  the  depletion.  As  a  matter  of  fact  the  patient's  weakness 
is  due  to  his  circulatory  embarrassment,  and  experience  teaches 


THE  TREATMENT   OF   VALVULAR  HEART-DISEASE  493 

that  instead  of  being  enfeebled  to  the  degree  a  healthy  individual 
would  be  by  the  purgation,  the  cardiopatK  actually  finds  he  feels 
stronger  so  soon  as  the  primary  effect  of  the  catharsis  is  past. 
This  is  particularly  true  of  mitral  patients  to  whom  heroic  purga- 
tion is  specially  beneficial.  Although  in  the  case  of  Mrs.  F.  elat- 
erin  was  highly  successful,  still  it  is  so  drastic  that  now^adays  I 
generally  order  a  less  irritating  remedy.  The  best  hydragogue  is 
a  saturated  solution  of  sulphate  of  magnesia,  and  of  this  I  am 
accustomed  to  prescribe  a  tablespoonful  hourly  to  an  adult  until 
it  begins  to  exert  its  effect.  I  have  known  patients  to  take  as 
much  as  4  and  even  6  ounces  before  getting  appreciable  results. 
The  efficacy  of  the  remedy  is  enhanced  if  the  patient  is  not 
allowed  to  follow  the  medicine  by  more  than  a  swallow  of  water — 
just  enough  to  remove  the  bitter  taste  of  the  salts.  If  it  is  com- 
plained that  the  drug  produces  a  bad  feeling  in  the  stomach,  this 
can  usually  be  counteracted  by  the  addition  to  each  dose  of  5  to  10 
drops  of  essence  of  Jamaica  ginger,  which  is  generally  found  in  the 
house.  Compound  jalap  powder  is  likewise  very  efficient  and  does 
not  prove  so  drastic  as  is  supposed.  Of  this,  a  heaping  teaspoon- 
ful  can  be  safely  given  to  an  adult  daily.  The  old-fashioned 
"  ten  ten,"  which  is  10  grains  each  of  calomel  and  jalap,  was 
much  employed  by  our  forefathers,  and  is  not  so  severe  as  it  is 
thought  to  be.  It  is  better,  however,  to  give  5  grains  of  calomel 
with  soda,  or  a  blue  pill  of  5  or  10  grains,  either  remedy  to  be 
followed  after  eight  or  ten  hours  by  ^  an  ounce  of  Epsom  or 
Rochelle  salts.  Bitartrate  of  potassium  is  also  a  capital  drug  for 
the  removal  of  dropsy,  and  by  some  patients  is  better  tolerated 
than  is  sulphate  of  magnesia.  Glauber's  salts  alone  is  too  disa- 
greeable, but  may  sometimes  be  combined  with  Epsom  salts  to 
advantage.  It  is  one  of  the  ingredients  of  Carlsbad  water,  by  the 
way.  Carlsbad  salts  are  often  prescribed  to  cardiac  patients,  but, 
to  be  very  efficient  for  the  removal  of  oedema,  has  to  be  given  in 
large  doses  dissolved  in  considerable  hot  water,  being  said  to  be 
more  efficacious  when  administered  warm.  If  copious  watery 
stools  are  to  be  secured,  it  is  best  to  prescribe  rather  concentrated 
remedies  and  not  allow  the  intake  of  much  water. 

In  case  such  energetic  catharsis  is  found  to  weaken  the  patient, 
his  strength  may  be  sustained  by  strychnine,  aromatic  spirits  of 
ammonia,  whisky,  or  some  other  stimulant.     Furthermore,   the 


494  DISEASES  OF   THE    HEART 

success  of  such  treatment  depends  not  alone  upon  its  vigour,  but 
also  upon  its  persistent  continuance,  day  after  day,  until  the 
upper-hand  has  been  gained  over  the  dropsy.  It  recpiires  judg- 
ment  and  courage  on  the  part  of  the  physician  and  fortitude  and 
faith  on  the  part  of  the  patient.  But  if  judiciously  persevered 
with,  it  generally  rewards  the  sufferer. 

The  Use  of  Digitalis. — When  at  length  venous  stasis  has  been 
diminished,  and  the  cardiac  cavities  have  been  relieved,  digitalis 
may  be  prescribed,  and  will  then  be  found  to  complete  the  good 
work  begun  by  the  cathartics.  The  beneficial  action  of  this  rem- 
edy is  generally  attributed  to  its  increasing  the  force  of  cardiac 
systoles,  in  consequence  of  which  the  arterial  system  becomes  bet- 
ter filled.  But,  as  suggested  by  Broadbent,  a  part  of  its  beneficial 
influence  is  to  be  found  in  the  greater  tonicity  imparted  to  the 
vessels  through  its  vaso-constricting  action.  With  improved  vas- 
cular tone,  blood-flow  is  hastened,  and  with  accelerated  circula- 
tion in  the  capillaries  and  lymphatics  absorption  of  transuded 
serum  is  promoted.  In  addition  digitalis  lengthens  diastole,  and 
thus  favours  the  emptying  of  the  pulmonic  veins,  right  heart,  and 
great  systemic  veins,  and  thus  counteracts  the  impending  stagna- 
tion of  the  circulation,  Blood-flow  in  the  renal  vessels  is  im- 
proved, and  forthwith  there  is  a  corresponding  improvement  in 
the  renal  function.  Accordingly,  as  previously  stated,  it  is  aug- 
mented diuresis  that  furnishes  the  most  reliable  token  of  the  bene- 
ficial action  of  digitalis. 

The  occurrence  of  dropsy  is  a  possibility  in  all  four  lesions  of 
the  left  heart,  but  is  far  less  often  seen  in  destroyed  compensation 
of  disease  of  the  semilunar  than  of  the  auriculo-ventricular  valve. 
Wlien,  however,  oedema  occurs  in  aortic-valve  lesions,  it  is  because 
dilatation  of  the  ventricle  has  led  to  relative  incompetence  of  the 
mitral  leaflets  with  back  pressure  in  the  ])ulmonic  system,  disten- 
tion of  the  right  heart,  and  the  establishment  of  a  condition  iden- 
tical with  that  of  uncompensated  primary  mitral  disease. 

In  cases,  therefore,  of  aortic  defects  manifesting  dropsy  the 
indication  is  for  the  administration  of  cathartics  and  digitalis  the 
same  as  in  mitral  disorders.  I  Ixdieve,  however,  that  the  latter 
should  be  administered  witli  judgnumt.  There  are  some  physi- 
cians who  advocate  the  employment  of  large  doses  of  digitalis  in 
all  cases  of  aortic  regurgitation  with  br(jken  compensation.     My 


THE   TREATMENT   OP   VALVULAR   HEART-DISEASE  496 

experience  leads  nie  to  agree  with  Broadbent  when  he  says  that 
a  distinction  should  be  made  between  cases  of  aortic  insufficiency 
with  ccdema  and  those  without.  When  loss  of  compensation  is 
shown  by  symptoms  pointing  to  left-ventricle  feebleness  rather 
than  by  oedema  and  back  pressure  consequent  upon  relative  mitral 
regurgitation,  then  I  am  emphatically  of  the  opinion  that  digi- 
talis must  be  given  with  caution.  It  is  quite  possible  in  such 
cases  for  digitalis  to  increase  peripheral  resistance  to  a  danger- 
ous degree  through  vascular  constriction.  Endoventricular  blood- 
pressure  is  correspondingly  raised,  and  if  the  ventricular  wall  is 
very  feeble,  unexpected  death  is  not  a  very  remote  contingency. 
In  such  cases,  therefore,  digitalis  should  be  given  cautiously,  and 
its  effects  should  be  attentively  watched. 

When,  on  the  other  hand,  droj)sy  is  present,  the  drug  may  be 
given  more  freely,  although  it  is  not  likely  to  accomplish  such 
brilliant  results  as  in  cases  of  mitral  disease.  Indeed,  it  has 
seemed  to  me  that  in  some  cases  of  aortic  insufficiency  with  sec- 
ondary mitral  leakage  large  doses  of  digitalis  actually  augmented 
pulmonary  and  right  heart  engorgement  by  driving  more  blood 
backward  through  the  mitral  than  forward  through  the  aortic  ori- 
fice. Such  certainly  was  the  effect  observed  in  the  case  narrated 
at  the  close  of  the  chapter  on  Aortic  Regurgitation.  Qi^dema  was 
not  present,  yet  the  state  of  the  heart  seemed  to  call  for  heroic 
doses  of  digitalis  in  the  forlorn  hope  of  lessening  the  dilatation  of 
the  left  ventricle.  Instead  of  doing  this,  however,  the  digitalis 
appeared  to  aggravate  back  pressure,  and  at  last  death  came  sud- 
denly and  unexpectedly. 

When  the  mitral  valve  has  given  way  in  cases  of  aortic  ob- 
struction there  is  still  less  prospect  of  reinstating  the  ventricle  by 
large  doses  of  digitalis.  The  impediment  to  outflow  into  the 
arterial  system  is  likely  to  cause  still  freer  reflux  into  the  auricle 
if  by  large  doses  of  digitalis  the  physician  attempts  to  force  the 
ventricle  beyond  a  certain  point. 

We  now  come  to  the  consideration  of  the  question  whether 
digitalis  is  equally  efficient  in  both  forms  of  mitral  disease. 
Broadbent  is  of  the  opinion  that  foxglove  manifests  its  happiest 
results  in  mitral  regurgitation,  whereas  in  mitral  constriction  the 
medicine  is  not  always  well  tolerated.  This  difference  is  due, 
he  holds,  to  the  fact  that  the  narrowing  of  the  oriflce  interferes 


496  DISEASES  OF   THE   HEART 

with  the  aspiration  of  blood  out  of  the  lungs  which  follows  the 
better  emptying  of  the  ventricle  produced  by  digitalis.  This  argu- 
ment applies  cogently,  no  doubt,  to  cases  of  extreme  stenosis  in 
which  the  orifice  is  reduced  to  a  mere  buttonhole  slit,  for  it  is  evi- 
dent that  in  such  an  extreme  condition  no  agent  can  drive  or  coax 
an  adequate  volume  of  blood  past  the  barrier.  Nevertheless,  ex- 
perience teaches  that  even  in  such  cases  digitalis  is  useful  if  prop- 
erly given.  This  is  in  accord  with  the  following  consideration: 
Digitalis  prolongs  diastole,  and  thus  affords  more  time  for  the 
stream  pent  up  in  the  auricle  to  flow  into  the  ventricle,  and  hence 
to  be  expelled  with  the  next  ensuing  systole.  Inasmuch,  however, 
as  the  capacity  of  the  left  ventricle  is  reduced-  in  pronounced  ste- 
nosis of  the  mitral  ring,  the  blood-wave  thrown  into  the  aorta  is 
of  a  necessity  small,  and  mammoth  doses  of  digitalis  are  not 
likely  to  accomplish  more  than  moderate  ones.  If  the  beneficial 
influence  of  this  remedy  were  limited  to  the  left  ventricle,  the 
usefulness  of  the  drug  would  bo  limited  indeed  in  these  cases. 
But  it  acts  also  on  the  right  ventricle  and  left  auricle,  and  by 
strengthening  the  vigour  of  their  contractions  it  enables  these 
chambers  to  exert  greater  propulsive  force.  In  the  light  of  these 
considerations  it  would  be  a  grave  mistake  to  conclude  that  this 
remedy  is  of  no  value  in  mitral  stenosis  even  when  broken  com- 
pensation has  led  to  a3dema  and  other  signs  of  serious  stasis. 
The  combined  use  of  depleting  measures  and  digitalis  will  some- 
times achieve  gratifying  results.  Fortunately  stenosis  and  regur- 
gitation are  often  conjoined  at  the  mitral  oritlce,  and  hence  such 
cases  are  to  be  treated  as  if  only  insufficiency  were  present. 

When,  therefore,  digitalis  is  to  be  employed  for  the  relief  of 
dropsy  due  to  ruptured  compensation  in  mitral  disease,  it  is  to  be 
given  in  large  and,  as  Balfour  says,  "  cumulating  "  doses.  They 
must,  however,  be  carefully  watched,  and  the  remedy  must  be 
stopped  so  soon  as  signs  of  its  toxic  action  are  perceived.  It  is 
my  habit  in  such  cases  to  administer  ^  an  ounce  of  the  fresh 
infusion  every  four  hours  for  four  or  five  days.  If  it  is  employed 
in  this  maimer,  and  if  it  is  witlidrawu  so  soon  as  the  increased  diu- 
resis first  ])i'o(luced  l)Ogins  to  be  succeeded  by  a  diminution  in  the 
amount  of  urine,  there  is  ordinarily  no  danger  of  serious  cumula- 
tive effects.  If  for  some  n^ason  the  drug  does  not  exhibit  its 
diuretic  action,  although  slowing  of  the  jnilse  is  obtained,  then 


THE   TREATMENT   OF   VALVULAR  HEART   DISEASE         497 

the  remedy  should  bo  stopped  for  a  day  or  two,  after  which  it  may 
again  be  given  in  smaller  doses.  There  is  no  use  in  administering 
digitalis  for  the  relief  of  oedema  in  small  doses  over  a  long  time. 
I  have  frequently  seen  it  fail  when  thus  given,  whereas  subse- 
quently prescribed  in  large  doses  during  several  days  it  has  suc- 
ceeded in  accomplishing  what  it  previously  failed  to  do. 

Finally,  I  wish  to  again  emphasize  the  statement  that  if  this  un- 
rivalled agent  is  to  be  employed  for  the  removal  of  oedema  it  is  best 
given  as  an  infusion  of  the  English  leaves.  The  tincture,  the  fluid 
extract,  or  the  powder,  digitoxine,*  and  the  various  digitalins, 
whether  French  or  German,  will  not  prove  so  efficient.  The  tincture 
is  preferable  for  prolonged  administration  in  small  tonic  doses.  It 
will  undoubtedly  augment  the  flow  of  urine  by  energizing  cardiac 
contractions,  but  for  the  removal  of  oedema  would  have  to  be  given 
in  doses  that  would  be  dangerous  in  the  hands  of  the  average  medi- 
cal man.  This  is  particularly  true  of  digitoxine  and  the  French  or 
crystallized  digitalia.  Excepting  the  latter,  I  have  tried  all  forms 
of  the  drug,  and  I  think  I  can  safely  assert  that  all  can  be  accom- 
plished with  the  reliable  tincture  and  properly  prepared  effusion 
that  can  be  with  the  other  less  familiarly  known  preparations.  I 
well  remember  my  experience  with  digitoxine.  In  one  case  it  pro- 
duced so  powerful  an  effect  in  what  was  considered  a  safe  dose,  that 
I  speedily  discontinued  it  in  alarm.  In  the  second  case,  that  of  a 
middle-aged  woman  with  mitral  disease  and  an  arrhythmic  pulse, 
the  remedy  was  administered  cautiously  and  without  appreciable 
effect  one  way  or  the  other,  when  suddenly,  almost  without  warning, 
the  patient  died.  I  could  not  say  her  death  was  due  to  the  digitox- 
ine, and  yet  I  have  always  had  an  uncomfortable  s"_spicion  that  it 
was.  Therefore  I  would  urge  inexperienced  practitioners  or  such 
as  practice  in  the  country,  where  they  cannot  keep  their  patients 
under  as  close  scrutiny  as  if  they  were  near  at  hand — in  a  hos- 
pital, for  instance — to  content  themselves  with  safer  preparations. 

Strophanthus,  convallaria  majalis,  adonis  vernalis,  erythro- 
jDhlein,  and  barium  chloride  belong  to  the  digitalis  group,  and 
therefore  possess  diuretic  properties,  convallaria  having  been 
particularly  lauded  by  the  Kussians.     ISTone  of  them  is  the  equal 

*  Since  June,  1906, 1  have  made  frequent  use  of  an  imported  solution  of  digitox- 
ine with  highly  gratifying  results  in  both  regulating  the  heart  and  increasing  the 
amount  of  urine. 
33 


498  DISEASES  OF  THE  HEART 

of  digitalis,  however,  and  in  serious  eases  they  are  not  likely  to 
prove  so  reliable.  I  have  used  them  as  adjuncts  or  substitutes  for 
foxglove  when  this  had  to  be  discontinued  temporarily  or  could 
not  be  tolerated,  but  I  have  never  ventured  to  rely  on  any  one  of 
them  exclusively  when  dealing  with  a  critical  ease  of  cardiac  in- 
competence from  valvular  disease.  In  the  young  with  rheumatic 
endocardial  lesions,  or  in  older  persons  whose  arteries  are  not 
aj^preciably  stiff,  one  need  not  apprehend  ill  effects  from  the  vaso- 
constrictor effect  of  digitalis,  while  if  the  remedy  be  given  in 
ice-water,  or  if  the  fat-free  tincture  be  used,  it  will  rarely  disa- 
gree seriously  with  the  stomach.  When  the  vessels  are  athero- 
matous its  effect  on  the  arteries  must  be  reckoned  with,  and  then 
strophanthus  may  have  to  be  used  instead  or  be  combined  with 
digitalis.  In  these  cases  the  latter  can  generally  be  employed 
sucecssfully  even  for  the  treatment  of  oedema  if  nitroglycerin  be 
given  often  enough  to  counteract  the  constriction  of  the  arterioles. 
Before  concluding  the  subject  of  the  administration  of  digi- 
talis I  wish  to  direct  attention  to  the  possibility  of  its  occasioning 
mental  symptoms  that  may  be  misunderstood  and  attributed  to 
the  disease  instead  of  to  its  right  cause.  These  are  hallucinations 
and  delirium.  II.  O.  Hall  has  recently  contributed  a  paper  on 
this  peculiar  action  of  the  drug,  and  quotes  from  an  article 
thereon  by  Duroziez,  who  reported  twenty  instances  of  the  kind. 
In  this  present  work  I  have  referred  to  the  fact  tliat  in  two  pa- 
tients whom  I  attended  in  connection  with  Dr.  Houston  a  peculiar 
mental  and  emotional  state  developed  during  the  prolonged  admin- 
istration of  digitalis  and  disappeared  after  the  discontinuance  of 
the  remedy.  In  Miss  T.,  with  mitral  disease,  there  was  a  singular 
sort  of  sullen  moroseness  with  taciturnity,  while  the  other  patient, 
a  man  with  aortic  insufficiency,  manifested  a  mild  delirimn  of  a 
harmless  kind.  Hall  suggests  that  this  effect  may  follow  tlie  ad- 
ministration of  even  moderate  doses  for  a  considerable  ])eri()d,  and 
very  properly  queries  if  it  does  not  occur  far  oftener  than  is  sus- 
pected. For  my  part  I  frankly  confess  that  until  my  attention 
was  directed  to  this  singular  effect  of  digitalis  by  Dr.  Houston  I 
had  no  suspicion  of  its  possibility.  Tliere  may  be  no  danger  asso- 
ciated with  this  action,  but  it  may  iudiciite  an  unusual  degree  of 
susceptibility  to  its  influence,  and  tliiif  in  such  ])ersons  one  should 
be  especially  on  his  guard  against  the  cnniulative  action  of  the 


THE   TREATMENT   OP  VALVULAR   HEART-DISEASE  499 

agent.  This  latter  is  no  fancied  one,  and  should  always  be  kept 
in  mind. 

It  is  probable  that  digitalis  poisoning  occurs  far  more  fre- 
quently than  is  suspected.  I  am  painfully  certain  that  in  one 
instance  the  sudden  death  of  one  of  my  patients  was  due  to  digi- 
talis, which  was  being  administered  in  large  doses.  In  this  case, 
however,  the  patient  disobeyed  my  emphatic  injunction  to  remain 
absolutely  quiet  in  bed,  and  fell  dead  while  walking  about,  just  as 
I  had  warned  him  he  might  do  if  he  got  up.  Since  that  time  it 
has  been  my  custom  to  discontinue  digitalis  every  fifth  or  sixth 
day  in  all  cases  in  which  it  is  being  taken  in  considerable  doses  or 
wheu  the  patients  are  not  under  frequent  observation.  In  this 
way  time  is  allowed  for  the  elimination  of  the  drug.  Lastly,  it  is 
said  that  there  is  less  danger  of  a  cumulative  eifect  if  a  daily 
cathartic  is  taken,  since  it  may  be  largely  eliminated  through  the 
bowels. 

Accessory  Heart-tonics — Strychnine  is  a  valuable  heart-tonic 
at  all  times,  and  when  compensation  is  lost  is  of  great  value.  It 
should  not  be  depended  on  alone,  but  prescribed  as  an  adjuvant  to 
the  cardiac  energizers  already  luentioned.  Administered  hypo- 
dermically  it  is  undoubtedly  more  rapid  and  powerful  than  by  the 
mouth,  and  would  best  be  employed  in  that  manner.  Its  bene- 
ficial action  is  not  confined  to  the  heart,  for  it  is  a  respiratory 
stimulant  as  well,  tending  thereby  to  lessen  the  sense  of  dyspnoea. 
Through  its  powerful  effect  as  a  tonic  to  the  nervous  system  it 
induces  a  feeling  of  strength  and  well-being  very  soothing  to  the 
tired,  often  irritable  sufferer.  It  certainly  helps  a  patient  endure 
the  insomnia  that  so  often  attends  his  loss  of  compensation. 

I  have  always  been  of  the  opinion  that  to  display  its  kindly 
action  strychnine  should  be  given  in  full  doses,  care  being  had 
to  avoid  its  physiological  effects  in  toxic  amounts.  One  thirtieth 
of  a  grain  hypodermically  may  usually  be  administered  every 
four,  or  in  extreme  cases  every  three  hours.  I  have  not  hesitated 
to  order  that  dose  as  often  as  every  two  hours,  or  even  hourly  in 
times  of  great  peril.  The  objection  to  such  doses  have  been  previ- 
ously stated.     (See  page  44.5.) 

Another  remedy  of  inestimable  service  when  the  heart  threat- 
ens to  fail  altogether  or  the  patient  is  tormented  by  dyspnoea,  par- 
ticularly at  night   (cardiac  asthma),  is  morphine.     If  adminis- 


500  DISEASES  OP  THE   HEART 

tcred  hypodermically  and  in  small  doses  this  drug  proves  a  pow- 
erful cardiac  stimulant.  An  eighth  or  a  tenth  of  a  grain  thrown 
under  the  skin  will  arouse  a  flagging  heart,  steadying  its  action 
and  improving  the  quality  of  the  pulse  in  a  manner  not  equalled 
by  any  other  agent  of  which  I  am  aware.  If  -j^  of  atropine  is 
combined  it  serves  to  warm  up  the  skin  by  flushing  the  capillaries, 
and  by  deepening  the  respirations  relieves  dyspnoea.  Given  at 
bedtime,  morphine  will  generally  carry  the  sufl"erer  through  the 
night  without  his  wonted  attack  of  dyspnoea  and  depression.  In 
some  instances  it  acts  as  a  hyjmotic,  but  even  when  it  fails  of  this 
action  it  allays  restlessness  and  induces  a  sense  of  well-being  that 
is  most  grateful.  Larger  doses  are  more  or  less  depressing,  and 
exhibited  by  the  mouth  the  stimulating  action  of  the  remedy  is  not 
the  same  as  by  subcutaneous  injection.  I  have  known  many  a 
patient  to  tolerate  morphine  in  this  manner  for  weeks,  and  when 
it  was  at  length  withdrawn  not  to  experience  any  special  discom- 
fort. It  is  not  to  be  resorted  to  indiscriminately,  but  only  in 
those  cases  in  which  it  is  necessary  either  to  tide  over  a  period 
of  crisis  or  to  promote  comfort  of  body  and  repose  of  spirit.  Of 
course  for  the  relief  of  pain  larger  doses  are  necessary,  as  is  like- 
wise the  ease  when  it  is  desired  to  produce  sleep. 

Hypnotics. — The  ultimate  aim  of  treatment  in  the  stage  we 
are  now  considering  is  the  restoration  of  circulatory  equilibrium, 
and  thereby  of  heart-power,  and  yet  we  should  never  forget  that 
the  accomplishment  of  our  aim  often  depends  almost  as  much 
upon  attention  to  subordinate  or  accessory  conditions  as  upon 
measures  addressed  to  the  heart  directly.  For  instance,  cardio- 
paths  suffering  from  ruptured  compensation  are  very  apt  to  com- 
plain of  actual  insomnia  or  of  fitful  and  unrefreshing  sleep.  This 
may  be  due  to  disturbed  cerebral  circulation,  to  retention  of  waste 
products,  or  to  the  generation  of  toxines,  or  to  all  these  factors 
combined.  So  long  as  natural  sleep  is  wanting,  the  invalid  is  de- 
j)rived  of  what  Shakespeare  has  so  fitly  termed  "  Nature's  sweet 
restorer,"  and  the  exhaustion  of  ilie  nerve-centres . following  pro- 
longed wakefidness  may  throw  the  balance  against  recovery. 
Moreover,  the  heart  itself  is  robbed  of  the  rest  which  comes  from 
its  slower  action  during  sleep.  It  is  most  important,  consequently, 
to  combat  this  distressing  condition  by  such  means  as  will  prove 
harmless. 


.   THE   TREATMENT   OF   VALVULAR  HEART-DISEASE  501 

In  some  cases  sleep  follows  the  measupes  directed  against  vis- 
ceral congestion  and  oedema,  or  is  directly  induced  by  the  hypo- 
dermics of  morphine  administered  for  relief  of  nocturnal  dysp- 
noea. When  such  is  not  the  case,  recourse  should  be  had  to  hyp- 
notic remedies  as  such. 

Chloral  hydrate  is  too  powerful  a  cardiac  depressor  to  be 
safely  employed  in  uncompensated  valvular  disease,  or  indeed  in 
any  case  in  which  the  pulse  is  not  strong  and  tense.  On  the  other 
hand,  chloralamide-Bayer  is  said  to  exert  no  injurious  effect  on  the 
circulatory  apparatus.  If  it  affects  the  pulse  at  all,  it  is  by  accel- 
erating it  while  at  the  same  time  augmenting  its  tension.  The 
main  draw^back  to  this  agent  is  its  liability  to  occasion  headache 
next  morning  and  its  unpleasant  acrid  taste.  To  obviate  the  for- 
mer effect,  therefore,  an  equal  amount  of  potassium  bromide  may 
be  added  to  each  dose  of  chloralamide,  while  its  disagreeable  taste 
may  be  disguised  by  some  palatable  sirup.  The  remedy  is  per- 
fectly safe  in  doses  of  from  15  to  40  grains,  and  to  prove  efficient 
ought  to  be  given  in  a  single  full  dose.  A  good  formula  is  the 
following:  Chloralamide-B.  2  grammes,  spiritus  frumenti  15 
cubic  centimetres,  potassii  bromidium  2  grammes,  and  syrupus 
glycyrrhiza^,  q.  s.,  ad  30  cubic  centimetres.  M.  et  sig.  This  dose 
to  be  taken  at  bedtime. 

Chloralose  is  a  hypnotic  highly  recommended  by  Balfour  in 
his  capital  work  The  Senile  Heart.  Its  dose  is  from  2  to  8  grains, 
best  given  in  capsule,  and  is  said  to  tend  to  slowing  of  the  pulse 
while  at  the  same  time  lowering  its  tension.  I  formerly  pre- 
scribed it  a  good  deal,  but  ultimately  abandoned  it  because  I 
found  that  when  my  lady  patients  took  5  grains  at  a  single  dose, 
or  were  obliged  to  repeat  a  capsule  containing  2|  to  3  grains,  they 
were  apt  to  complain  of  nervousness  the  next  morning ;  it  is,  how- 
ever, safe  and  usually  produces  sleep  quickly.  Sulphonal  and  tri- 
onal  are  both  safe  and  efficient  hypnotics  for  the  class  of  cases 
now  considered,  since  although  they  accelerate  the  pulse  and 
somev\diat  raise  arterial  tension,  they  do  not  depress  the  heart. 
Paraldehyde  in  full  medicinal  doses  of  a  drachm  acts  similarly 
to  chloral  hj^drate  as  a  soporific,  but  unlike  the  latter  is  perfectly 
safe  even  for  weak  hearts,  being  said  to  slow  and  strengthen  the 
pulse.  Its  action  is  not  so  prolonged,  however,  and  patients  often 
object  to  it  on  account  of  its  burning  taste  and  persistent  odour 


502  DISEASES  OF  THE   HEART 

in  the  breath.  This  does  not  by  any  means  complete  the  list  of 
available  hypnotic  remedies,  but  comprises  those  that  are  the  most 
efficient  for  cardiac  sufferers.  Should  these  not  occasion  sleep, 
and  in  uncompensated  valvular  lesions  insomnia  is  often  most 
intractable,  recourse  would  better  be  had  to  morphine  or  some 
preparation  of  opium,  of  the  advantages  of  which  as  a  heart-tonic 
I  have  already  spoken. 

Rest. — Having  dwelt  at  some  length  on  the  medicinal  manage- 
ment of  this  stage  of  valvular  heart-disease,  1  now  desire  to  add  a 
few  remarks  concerning  the  great  importance  of  physical  repose. 
Nothing  is  more  essential  when  compensation  has  failed  than  the 
strict  enforcement  of  absolute  rest.  There  is  no  greater  mistake, 
and  nothing  that  will  more  surely  render  futile  all  attempts  to  re- 
move dropsy,  than  to  permit  the  patient  to  walk  about.  Even  the 
moderate  exertion  of  visiting  the  closet  in  an  adjoining  room  will 
often.be  sufficient  to  maintain  the  venous  congestion  and  a'dema. 
The  patient  should  be  required  to  remain  absolutely  in  bed  or  on 
a  couch,  and  he  should  make  use  of  a  bed-pan.  Only  in  those 
instances  in  which  ])aticnts  find  it  impossible  to  so  empty  the 
bowel  or  bladder  should  this  rule  find  an  exception.  When  such 
is  the  case,  they  may  be  permitted  to  leave  their  bed  and  sit  upon 
a  night-stool  placed  close  at  hand,  or  better  still  use  an  adjustable 
bed.  The  effort  of  raising  themselves  in  bed  will  often  in  cases 
of  extreme  dilatation  suffice  to  frustrate  all  attempts  at  a  reduc- 
tion in  the  size  of  the  organ.  Therefore,  dropsical  patients 
should  have  the  necessity  of  physical  repose  clearly  explained  to 
them,  and  should  be  kept  at  rest  until  all  traces  of  oedema  have 
disappeared.  In  mitral  disease  this  precaution  will  of  itself  often 
do  much  towards  removing  symptoms.  In  cases  of  uncompensated 
aortic  insufficiency  al)solute  re])Ose  is  of  the  utmost  importance, 
since  a  single  injudicious  effort  may  occasion  paralysis  of  the 
overdistended  left  ventricle  in  diastole. 

Another  danger  arising  from  exertion  in  cases  of  extreme  and 
long-continued  back  pressure  in  the  lungs  is  the  establishment  of 
relative  pulmonary  regurgitation.  When  this  once  supervenes,  it 
is  in  my  experience  impossible  to  ever  again  restore  compensa- 
tion, and  the  end  is  not  far  distant. 

Exercise. — Only  after  the  cardiac  cavities  have  become  un- 
loaded, and  compensatory  hypertrophy  has  begun  to  be  restored, 


THE   TREATMENT   OP   VALVULAR  HEART-DISEASE  503 

dare  the  patient  be  allowed  to  indulge  in  exercise.  Even  then 
exertion  must  be  very  slight  at  first,  and  the  medical  attendant 
should  observe  the  effects  of  effort,  and  thus  form  an  intelligent 
opinion  of  how  far  cardiac  strength  has  become  re-established.  I 
make  it  a  rule  to  be  present  the  first  time  walking  is  attempted, 
so  as  to  note  the  effect  of  exertion  on  the  pulse. 

Baths. — In  this  critical  stage  of  cardiac  incompetence  I  believe 
ISTauheim  baths  contra-indicated,  and  even  in  the  matter  of  bathing 
for  the  sake  of  cleanliness  patients  must  content  themselves  with 
the  morning  sponge-bath  given  by  the  nurse.  It  involves  too 
much  exertion  for  them  to  bathe  themselves,  and  particularly  to 
get  into  a  tub. 

Receiving  Visitors. — Aj)parently  trivial  influences  may  make 
for  or  against  the  restoration  of  heart-power.  Consequently,  when 
there  is  a  damming  back  of  the  blood  into  the  lungs  and  right 
heart,  this  latter  chamber  should  not  be  additionally  strained  by 
prolonged  conversation.  The  reason  for  this  lies  in  the  consid- 
eration that  when  words  are  uttered  the  breath  is  held,  and  that 
with  expiratory  effort  air  is  driven  out  through  the  partially 
closed  glottis.  That  this  throws  additional  burden  on  the  heart 
is  plain,  and  is  proved,  moreover,  by  the  clinical  observation  that 
cardiopaths  nearly  always  exhibit  breathlessness  while  talking. 
Therefore,  these  invalids  should  not  be  allowed  to  receive  visits 
from  friends,  unless  perhaps  from  a  few  who  can  be  relied  on  to 
monopolize  the  conversation,  and  who  know  enough  to  leave  so 
soon  as  the  patients  exhibit  signs  of  w^eariness. 

Diet. — This  is  a  matter  of  the  very  greatest  importance,  and 
must  not  be  left  to  the  whims  of  the  invalid  or  the  zealous  but 
ignorant  notions  of  friends.  The  considerations  and  principles 
which  obtain  in  cases  of  failing  but  not  yet  wholly  lost  heart- 
power  apply  with  added  emphasis  to  these,  and  hence  the  reader 
is  referred  to  what  has  been  already  said. 

Although  the  management  of  this  stage  of  valvular  lesions  is 
to  be  conducted  along  definite  lines,  still  it  is  and  must  of  a  neces- 
sity be  largely  symptomatic.  There  is  a  certain  routine  about  it, 
and  yet  the  physician  must  be  ever  alert  to  detect  signs  of  danger 
and  avert  it  by  prompt  action,  and  equally  to  take  advantage  of 
all  circumstances  that  exert  an  influence  for  good.  He  should 
not  exhaust  his  patient  by  unnecessary  examinations,  and  yet  he 


504  DISEASES   OF   THE   HEART 

should  look  over  the  case  daily  with  sufficient  care  to  detect  the 
earliest  signs  of  any  of  the  man}'  complications  to  which  the 
patient  is  liable.  It  is  especially  necessary  to  make  frequent  and 
thorough  analyses  of  the  urine,  and  he  should  insist  on  a  record 
being  kept  of  the  temperatiire  for  the  detection  of  some  of  the 
terminal  infections  so  frequent  in  these  cases.  If  he  cannot 
restore  cardiac  energy,  he  can  at  least  prolong  life  and  do  much 
to  minister  to  the  patient's  comfort. 

If  he  be  so  fortunate  as  to  aid  Nature  in  re-establishing  some 
degree  of  cardiac  power,  the  case  then  becomes  one  of  the  second 
class,  and  is  to  be  managed  along  the  lines  laid  down  in  the  second 
portion  of  this  chapter. 


SECTION  III 
DISEASES   OF   THE   MYOCARDIUM 


CHAPTER   XIX 
ACUTE    MYOCARDITIS 

It  is  not  the  design  in  this  chapter  to  consider  acute  inflam- 
mation of  the  myocardium  in  association  with  acute  peri-  or  endo- 
carditis, but  the  acute  inflammation  observed  in  the  course  of  spe- 
cific fevers  and  other  acute  infectious  processes,  and  which  usu- 
ally exists  independently  of  inflammation  of  those  membranes. 
This  form  of  myocarditis  is  described  by  authors  as  acute  intersti- 
tial and  acute  parenchymatous  myocarditis,  the  latter,  as  re- 
marked by  Osier,  being  regarded  by  some  as  a  degenerative 
process. 

The  history  of  acute  myocarditis  is  not  clear  until  we  come  to 
the  works  of  comparatively  recent  years.  Suppurative  myocar- 
ditis has  been  recognised  since  the  earliest  days  of  medicine,  and 
by  Galen  was  regarded  as  the  disease  of  gladiators  (Huchard). 
Beniveni,  in  the  fifteenth  century,  discovered  an  abscess  in  the 
wall  of  the  left  ventricle,  and  in  1553  Nicolas  Massa  found  an 
abscess  in  the  right  ventricle  with  a  sinuous  tract  extending  into 
and  perforating  the  auricle. 

Morgagni  was  familiar  with  myocardial  inflammation,  and 
Senac  devoted  a  chapter  to  this  affection. 

Since  the  beginning  of  the  last  century  the  names  of  innumer- 
able workers,  including  Corvisart,  Hope,  Andral,  Laennec,  and 
Stokes  are  linked  with  the  history  of  myocarditis,  but  their  views 
were  more  or  less  obscure.  For  the  most  part  the  changes  were 
spoken  of  as  a  softening  of  the  heart-muscle. 

Bouillaud  considered  this  softening  as  due  to  infl^ammation  of 
34  505 


506  DISEASES  OF  THE  HEART 

both  the  muscle-fibres  and  interstitial  connective  tissue,  and  dis- 
tinguished three  varieties:  The  red,  which  is  acute;  the  white  or 
gray,  which  is  purulent ;  and  the  yellow,  which  is  a  chronic  phleg- 
masia. 

Rokitansky  distinguished  acute  interstitial  and  acute  paren- 
chymatous myocarditis,  and  gave  an  excellent  description  of  them 
as  he  observed  them  in  cases  of  typhus  fever. 

Virchow's  studies  on  parenchymatous  myocarditis  opened  a 
ncAv  era,  for  in  place  of  the  old-time  changes  in  the  consistency 
of  the  heart-muscle  he  described  definitely  recognisable  micro- 
scopic and  chemical  changes  in  the  structure  of  the  muscle-fibres. 
lie  was  followed,  in  Germany,  by  Stein,  von  Zenker,  and  others, 
while  in  France,  Hayem  did  noteworthy  work  along  the  same 
lines.  The  three  divisions,  which  Hayem  made  according  to  the 
duration  of  the  process,  were  thought,  how^ever,  to  be  too  sharply 
drawn. 

Among  more  recent  German  writers  who  have  made  valuable 
contributions  to  acute  myocarditis  as  observed  particularly  in 
diphtheria,  are  to  be  found  the  names  of  Birch-IIirschfeld,  Ley- 
den,  Rosenbach,  and  Romberg.  Tlie  last-named  is  considered  by 
Fraentzel  to  have  added  greatly  to  our  knowledge  on  this  subject, 
and  I  desire  to  acknowledge  my  indebtedness  to  his  lucid  and 
eminently  practical  exposition  of  the  clinical  features  of  acute 
myfx'urditis,  as  .set  forth  in  Ebstein's  Practice. 

Morbid  Anatomy. — The  myocardium  is  the  muscle  layer 
of  the  heart,  and  corresponds  to  the  media  of  the  arteries.  It  is 
tliick  in  the  walls  of  the  ventricles  and  thinner  in  those  of  the 
auri(*les. 

The  lesions  of  myocarditis  are  usually  most  pronounced  in  the 
ventricular  walls  on  account  of  the  greater  work  thrown  on  these 
portions  of  the  heart-muscle.  The  fibre  of  the  heart-muscle  is 
structurally  between  that  of  voluntary  and  involuntary  muscle. 
The  individual  cells  are  short  cylindrical  bodies,  containing  one 
nucleus  each.  The  greater  portion  of  the  protoplasm  is  differen- 
tiated into  contractile  fibrilkc  which  possess  the  optical  character- 
istics necessary  to  give  the  appearance  of  striation,  the  fibre  being 
thus  striated  in  both  the  cross  and  longitudinal  direction. 

The  myocardium  possesses  a  very  rich  capillary  blood-supply 
which  is  derived  from  the  coronary  arteries,  and  also  from  minute 


ACUTE*  MYOCARDITIS  507 

arteries  opening  directly  from  the  left  ventricle.  Normally  there 
is  but  little  interstitial  tissue  in  the  myocardium,  which  is  sepa- 
rated from  the  pericardium  by  a  variable  layer  of  fat,  while  the 
endocardium  lies  directly  on  the  muscle  layer. 

Acute  myocarditis  is  either  parenchymatous  or  interstitial. 
The  parenchymatous  form  includes  the  various  acute  degenera- 
tions of  the  myocardium,  which  are  usually  dependent  on  the 
presence  of  irritants  in  the  circulation,  such  as  the  toxines  of  the 
infectious  fevers.  Cloudy  swelling  and  granular  degeneration 
are  the  most  common  manifestations  of  the  process.  In  them  the 
myocardium  appears  pale  and  opaque,  and  is  soft,  flabby,  and 
easily  torn. 

Microscopically  the  fibres  are  swollen,  their  protoplasm  more 
or  less  granular,  and  both  the  cross  and  longitudinal  striations  are 
obscured.  The  degeneration  induces  a  more  fragile  condition  of 
the  fibres,  so  that .  they  are  often  found  ruptured  or  separated 
along  the  cell  boundaries — a  condition  of  fragmentation  or  seg- 
mentation. In  these  cases  the  rupture  probably  takes  place  in 
articulo  mortis.  Both  these  forms  of  degeneration  are  usually 
diffuse  and  not  confined  to  any  special  areas. 

A  form  of  acute  myocarditis  which  may  be  classed  as  paren- 
chymatous, and  which  sometimes  leads  to  serious  results,  is  that 
which  follows  embolism  of  the  coronary  arteries.  Infarction  of 
the  heart  is  followed  by  coagulation  necrosis  of  the  tissue  involved, 
and  is  usually  attended  by  some  inflammatory  infiltration  of  the 
area.  Ultimately  the  necrotic  area  is  replaced  by  scar  tissue  in 
the  manner  to  be  considered  under  the  heading  of  the  chronic 
form  of  the  disease. 

Acute  interstitial  myocarditis  may  be  purulent  or  simple.  The 
purulent  form  is  usually  characterized  by  the  formation  of  ab- 
scesses, which  may  be  many  or  few  in  number.  On  section  these 
appear  as  whitish  or  grayish  areas  of  softening,  which  are  de- 
pressed below  the  plane  of  the  cut.  The  larger  abscesses  may  con- 
tain fluid  or  semi-fluid  pus. 

Often  associated  with  acute  endocarditis,  it  may  be  a  direct 
extension  from  the  disease  of  the  endocardium.  In  this  case  the 
foci  of  suppuration  are  larger  and  less  numerous  than  in  the  case 
of  suppurative  myocarditis  dependent  on  a  general  pysemia  when 
the  foci  are  numerous,  widely  scattered,  and  may  be  so  small  as  to 


508  DISEASES  OF  THE  HEART 

be  barely  visible  to  the  unaided  eye.  Microscopically  the  smaller 
foci  appear  as  masses  of  polymorphonuclear  leucocytes  surrounded 
by  a  zone  of  degenerating  muscle. 

Bacteria  can  often  be  demonstrated  by  appropriate  methods. 
The  abscesses  rarely  attain  large  size  on  account  of  the  early  su- 
pervention of  death.  They  may  rupture  into  the  heart  or  into  the 
pericardium,  or  the  wall  may  become  so  weakened  as  to  produce 
rupture  through  the  entire  thickness  of  the  heart. 

The  simple  form  of  acute  interstitial  myocarditis  is  a  rare 
condition  which  is  found  in  some  of  the  infectious  diseases,  nota- 
bly typhoid  fever  and  diphtheria.  In  this  the  chief  lesion  is  the 
infiltration  of  the  tissue  with  lymphoid  and  plasma  cells.  These 
foci  of  infiltration  are  more  numerous  in  the  left  than  in  the  right 
ventricle,  and  are  usually  situated  close  beneath  the  endocardium. 
In  these  foci  of  infiltration  there  is  usually  considerable  degener- 
ation of  the  muscular  tissue,  which  is  characterized  by  swelling 
and  destruction  of  the  nuclei. 

Associated  with  acute  myocarditis  are  the  various  conditions 
to  which  the  disease  is  secondary.  Chronic  myocarditis  may 
often,  though  not  always,  be  secondary  to  the  acute  form.  In 
abscess  of  the  heart,  rupture  into  the  circulation  may  cause  gen- 
eral ])va'mia  and  septic  embolism. 

Etiology. — Acute  inflammation  of  the  heart-muscle  is  ob- 
served in  connection  with  such  acute  infectious  diseases  as  diph- 
theria, typhoid  and  typhus  fever,  small-pox,  scarlatina,  gonor- 
rhoea, and  even  articular  rheumatism. 

Freund  has  described  a  case  of  acute  diffuse  myocarditis  of 
the  purulent  variety  in  a  forty-eight-year-old  butcher  who  fur- 
nished no  evidence  either  before  or  after  death  of  any  other  infec- 
tion than  that  of  inflammatory  rheumatism.  He  also  cites  simi- 
lar instances  collected  from  the  literature.  Whether  in  cases  of 
rheumatic  arthritis  there  is  some  secondary  infection  that  is  re- 
sponsible for  the  myocarditis,  or  it  is  the  rheumatic  poison  itself 
that  creates  the  mischief,  it  is  impossible  to  decide.  In  the  spe- 
cific fevers  it  is  the  specific  infection  probably  which  gains  access 
to  the  heart-muscle  and  there  excites  inflammation.  It  may  also 
be  that  the  character  of  the  myocarditis  is  determined  by  the  viru- 
lence of  the  micro-organism.  Romberg  thinks  it  is  the  intensity 
of  the  poison  and  not  its  continued  action  which  determines  the 


ACUTE?  MYOCARDITIS  509 

ultimate  course  of  the  inflainniatory  process,  for  "  in  many  cases 
the  disease  of  the  heart-muscle  reaches  its  highest  point  a  consid- 
erable time  after  the  decline  of  the  infection,  and  it  is  not  to  be 
assumed  that  all  this  time  the  toxic  agency  continues  to  increase 
in  activity." 

The  process  may  possibly  be  compared,  he  thinks,  to  the  in- 
flammatory reaction  set  up  in  a  part  whose  function  has  been 
destroyed  by  a  burn,  or  to  the  tabes  dorsalis  which  develops  as  an 
after  effect  of  syphilitic  infection. 

In  May,  1900,  Poynton  reported  a  comparative  study  of  the 
changes  in  the  heart-wall  in  one  case  each  of  diphtheria,  rheuma- 
tism, and  chorea.  In  the  first-named  affection,  which  occurred  in 
a  child  of  five  years,  and  proved  fatal  on  the  seventeenth  day,  the 
changes  were  those  of  acute  parenchymatous  degeneration,  the 
muscle-fibres  showing  profound  destruction,  in  some  places  even 
to  the  disappearance  of  the  muscle-cells  with  retention  of  only  the 
reticulum.  Associated  therewith  was  a  cellular  infiltration  of  the 
interstitial  connective  tissue.  The  endocardium  and  pericardium 
were  free  from  disease. 

In  the  heart  of  the  rheumatic  patient,  a  young  man  with  clini- 
cal evidence  of  mitral  disease  on  admission,  and  a  day  or  two  later 
of  fresh  pericarditis,  which  lesions  were  found  after  death,  the 
muscle-fibres  showed  extensive  fatty  degeneration,  but  were  not 
so  profoundly  disintegrated  as  in  the  case  of  diphtheria.  There 
was  also  an  exudation  of  cells  into  the  connective  tissue  here  and 
there  around  the  blood-vessels. 

In  the  case  of  chorea,  a  child  that  had  manifested  great 
rapidity  of  cardiac  action,  the  muscle-fibres  of  the  heart  also 
showed  more  or  less  fatty  degeneration  with  scattered  areas  of  cell 
exudation  into  the  interstitial  connective  tissue.  The  changes 
resembled  those  found  in  the  heart  of  a  rabbit  that  had  been  ren- 
dered pya^mic  by  the  injection  into  the  circulation  of  streptococci. 

In  commenting  on  the  microscopic  findings  in  the  diphtheritic 
heart,  Poynton  pointed  out  their  close  similarity  to  those  de- 
scribed by  Mollet  and  Eegaud,  and  produced  by  the  injection  of 
diphtheria  toxines  into  lower  animals.  As  to  the  myocardial 
changes  in  the  rheumatic  case  Poynton  was  of  the  opinion  that 
they  were  without  doubt  due  to  the  rheumatic  poison,  and  that 
they   strongly   suggested   the  likelihood   of  the   rheumatic  virus 


510  DISEASES  OF  THE  HEART 

being  a  toxine  of  microbic  origin ;  their  clinical  significance  was 
very  obvious  and  proved  that  the  cardiac  failure  in  rheumatic  pa- 
tients with  valve  defects  is  not  always  to  be  attributed  to  mechan- 
ical causes. 

Whereas  these  observations  of  Poynton  are  not  new,  they  are 
of  value  because  contrasting  and  illustrating  the  effects  on  the 
myocardium  of  these  two  important  diseases,  diphtheria  and 
rheumatic  fever. 

Purulent  inflammation  of  the  myocardium  is  found  in  connec- 
tion with  pyipmia  and  ulcerative  endocarditis,  the  bacteria  being 
brought  to  the  heart-muscle  in  the  blood  or  gaining  access  directly 
from  the  endocarditic  affection.  Septic  emboli  may  enter  a 
coronary  artery  and  give  rise  to  abscesses.  The  primary  focus  of 
infection  may  be  a  suppurating  wound,  or  micrococci  may  effect 
an  entrance  into  the  system  without  leaving  any  trace  of  their 
port  of  entry  behind. 

In  rare  instances  acute  myocarditis  has  appeared  to  follow 
trauma,  as  in  a  case  reported  by  Rindfleisch  of  a  man  who  gave 
no  other  etiological  factor  than  a  fall  from  a  considerable  height, 
and  striking  on  the  left  side  of  his  chest. 

Symptoms. — The  observations  of  Romberg  and  Schmaltz 
have  shown  that  in  diphtheria  the  symptoms  of  acute  myocarditis 
occur  in  from  10  to  20  per  cent  of  all  cases,  and  in  the  majority 
of  instances  appear  in  the  second  or  third  week  of  the  illness, 
occasionally  towards  the  end  of  the  first,  and  rarely  as  late  as  the 
sixth  or  tenth  week.  These  symptoms  are  the  expression  of  dimin- 
ished heart-power,  and  naturally,  as  regards  intensity,  depend 
upon  the  degree  of  the  myocardial  inflammation.  Although  for 
the  most  part  they  are  so  apparent  that  they  cannot  escape  detec- 
tion by  a  careful  observer,  yet  there  are  cases  in  which  death 
takes  place  suddenly  without  previously  recognisable  symptoms. 
On  the  oth(!r  hand,  according  to  Romlierg,  the  symptoms  of  acute 
myocarditis,  when  occurring  in  typhoid  fever,  scarlatina,  small- 
pox, gonorrhoea,  and  acute  articular  rheumatism,  are  less  conspicu- 
ous than  those  of  diphtheria;  particularly  is  this  true  during  the 
stage  of  fever.  Furthermore,  it  is  often  impossible  without  post- 
mortem inspection  of  the  heart-muscle  to  determine  whether  the 
symptoms  are  not  due  merely  to  functional  derangement  of  the 
heart's  action. 


ACUTE  MYOCARDITIS  511 

In  all  cases  of  acute  myocarditis  which  is  not  purulent  it 
is  a  subject  for  sjDeculation  whether  the  weakening  of  cardiac 
energy  is  due  to  destruction  of  the  muscular  elements,  or  to 
the  mechanical  effect  of  cell  exudation  into  the  interstitial  con- 
nective tissue,  or  depends  merely  upon  functional  depression 
(Romberg). 

Subjective  symptoms  are  not  aways  present,  and  if  not  wholly 
lacking  are  not  always  pronounced,  and  therefore  close  observa- 
tion on  the  part  of  the  medical  attendant  should  never  fail.  Pal- 
lor of  the  countenance  is  present,  and  is  often  a  striking  phenome- 
non. Poynton  mentions  it  in  both  of  his  cases  of  diphtheria  and 
rheumatic  fever,  especially  the  former.  It  is  due,  according  to 
Romberg,  to  defective  filling  of  the  cutaneous  vessels,  since  the 
blood  is  of  normal  composition.  Vomiting  is  another  symptom 
sometimes  of  great  importance,  and  has  been  dwelt  on  by  Villy 
in  connection  with  the  cardiac  failure  of  diphtheria.  It  may  be 
so  persistent  as  to  suggest  some  abdominal  disorder.  There  is 
anorexia,  and  the  patient  is  often  strikingly  weak  and  listless,  or 
instead  of  apathy  may  display  restless  anxiety.  In  a  word,  the 
patient  conveys  the  impression  of  being  profoundly  ill. 

The  features  of  the  case,  however,  that  most  strongly  point  to 
myocarditis  pertain  to  the  seat  of  mischief — i.  e.,  the  heart.  The 
pulse  is  more  frequent  than  normal,  although  as  a  rule  its  rate  is 
not  greatly  accelerated,  being  100  or  thereabouts.  •  Arrhythmia 
may  or  may  not  be  present;  often  there  is  only  irregularity  in 
force  and  volume.  Its  striking  characteristics  are  feebleness  and 
emptiness,  and  as  the  disease  progresses  loss  of  stability  as  well 
as  volume,  very  slight  exertion  being  sufficient  to  send  up  the 
pulse-rate  out  of  all  proportion  to  the  degree  of  effort. 

Examination  of  the  heart  at  this  time  may  disclose  some  in- 
crease of  dulness,  particularly  of  the  relative,  to  the  left  and 
upward,  but  also  to  the  right.  Yet  in  the  beginning,  sometimes 
even  throughout  the  course  of  the  malady,  marked  dilatation  is 
not  detected.  Cardiac  impulse  is  absent,  and  the  sounds  are  nota- 
bly feeble,  especially  the  first  at  the  apex,  which  is  often  so  toneless 
as  to  be  almost  inaudible.  In  a  few  cases  dilatation  of  the  left  ven- 
tricle reaches  such  a  degree  as  to  permit  muscular  incompetence 
of  the  mitral  valves,  which  is  declared  by  a  soft,  it  may  be  feeble 
systolic  apex-murmur.     The  disturbance  of  the  circulation  may 


512  DISEASES  OF   THE   HEART 

be  further  shown  by  hepatic  engorgement,  and  in  some  cases 
patients  complain  of  pain  in  the  region  of  the  liver. 

The  presence  or  absence  of  other  signs  of  venous  stasis,  as 
oedema  and  scanty,  albuminous  urine,  is  determined  by  the  degree 
of  circulatory  embarrassment.  In  some  cases  there  is  much  pra3- 
cordial  oppression  and  anxiety  that  may  amount  even  to  pain  of 
a  dull  and  ojipressive  or  poignant  character.  Freund  lays  great 
stress  on  substernal  pain,  and  thinks  it  a  highly  significant  symp- 
tom and  far  more  pronounced  than  in  endocarditis.  In  his  case 
the  patient  often  indicated  the  sternal  region  as  the  seat  of  his  dis- 
comfort, and  declared  he  knew  he  was  going  to  die. 

The  course  of  acute  myocarditis  is  very  variable.  It  may  set 
in  abruptly  and  progress  rapidly  with  severe  symptoms,  leading 
to  death  in  two  or  three  days  or  one  or  two  weeks;  or  it  may 
arise  insidiously  and  be  latent  throughout,  even  up  to  the  moment 
of  sudden,  unexpected  deatli ;  or  there  may  be  alternation  of 
periods  of  entire  absence  of  subjective  symptoms,  with  times  of 
alarming  weakness  and  indications  of  threatening  dissolution. 

The  cases  which  in  one  sense  are  the  most  dangerous  are  those 
in  which  the  myocarditis  develops  weeks  after  the  disa])])oarance 
of  the  diphtheria,  at  a  time  when  convalescence  is  thought  to  be 
progressing  satisfactorily,  and  the  patient  has  perhaps  passed  out 
from  under  the  care  of  the  physician.  In  such  the  child,  uncon- 
scious or  uncomplaining  of  symptoms,  plays  about  as  usual,  and 
one  day  making  some  extra  exertion  falls  to  the  floor  and  exj)ires 
without  warning. 

Romberg  is  of  the  opinion  that  the  circulatory  disturbance  is 
not  to  be  explained  on  the  hypothesis  of  mechanical  obstruction 
merely,  the  same  as  in  cases  of  chronic  cardiac  disease,  inasmuch 
as  cyanosis,  dyspnoea,  and  (edema  are  not  prominent  symptoms. 
The  pallor  and  arterial  emptiness  af6  rather  the  eff"ects  of  the 
toxines  on  the  vaso-motor  centre,  of  the  kind  shown  by  his  and 
Passler's  experiments  to  result  froui  acute  infections.  It  is  pos- 
sible also  that  splanchnic  neuritis,  as  suggested  by  Veronese,  may 
be  a  factor,  producing  stasis  within  the  great  abdominal  vessels, 
paralysis  of  the  vagus  being  out  of  the  question.  Only  in  some 
such  way  can  one  account  for  the  absence  of  pulmonary  congestion 
and  dyspna-a. 

As    regards    myocarditis    from    rheumatic    fever,    it    usually 


ACUTE 'MYOCARDITIS  513 

attacks  hearts  already  the  seat  of  acute  or  chronic  endocarditis,  or 
is  associated  with  pericarditis,  although,  the  muscle  alone  may 
sometimes  be  affected.  For  this  reason  it  is  not  easy  to  recog- 
nise or  definitely  determine  the  myocarditic  complication.  More- 
over, experience  proves  the  folly  of  attributing  to  myocardial  in- 
flammation the  cardiac  asthenia,  or  even  dilatation,  so  often  wit- 
nessed in  acute  rheumatism,  for  it  is  often  but  a  manifestation 
of  the  poison  upon  the  function  of  the  organ.  At  all  events,  it  is 
the  part  of  wisdom  in  such  cases  to  refrain  from  a  positive 
opinion. 

In  typhoid  and  scarlet  fever  it  is  not  uncommon  to  observe 
during  the  height  of  the  attack  symptoms  of  heart  weakness, 
which  in  most  instances  subside  with  convalescence,  and  which 
are  perhaps  the  result  of  the  action  of  the  infection  on  the  vaso- 
motor centre  in  the  cord,  together  with  exhaustion  of  the  heart- 
muscle.  JSTevertheless,  one  should  guard  against  an  inclination  to 
look  on  all  such  manifestations  as  not  due  to  myocarditis.  The 
onset  of  acute  inflammation  of  the  heart-wall  is  often  so  insidious 
during  the  febrile  stage,  and  the  symptoms  are  so  latent,  that  the 
real  nature  of  the  heart  disorder  is  readily  overlooked. 

On  the  contrary,  when  after  subsidence  of  all  active  symptoms 
referable  to  the  primary  disease  and  during  convalescence  the 
pulse  begins  to  assume  the  characters  already  described — i.  e., 
feebleness,  emptiness,  irregularity,  and  conspicuous  instability — 
one  should  at  once  suspect  the  existence  of  myocarditis. 

We  frequently  encounter  individuals  who  have  successfully 
weathered  a  severe  typhoid  fever  many  months,  even  two  or  three 
years  before,  and  still  display  undue  rapidity  and  even  irritabil- 
ity of  the  heart's  action,  I  am  always  inclined  to  speculate  on  the 
possibility  of  such  patients  having  suffered  from  unsuspected 
myocarditis  of  mild  form,  and  yet  sufficient  to  have  left  its  traces 
behind.  Should  the  heart-muscle  become  inflamed  during  or  after 
the  subsidence  of  acute  rheumatic  manifestations,  the  symptoms 
of  circulatory  embarrassment  will  be  out  of  proportion  to  the 
clinical  evidence  of  cardiac  disease,  and  yet  are  very  likely  to  be 
attributed  to  such  structural  alterations  as  are  discovered.  There 
is  far  more  feebleness,  emptiness,  inequality,  perhaps  intermit- 
tence,  and  particularly  instability  of  the  pulse,  than  there  is  evi- 
dence of  visceral  engorgement  and  mechanical  obstruction  in  the 


514:  DISEASES  OF  THE  HEART 

extremities,  at  all  events  until  sufficient  time  has  elapsed  for  the 
endocardial  mischief  to  become  intensified  by  the  myocarditis. 

The  sjinptoms  of  j)urulent  myocarditis  depend  somewhat 
upon  the  nature  and  extent  of  the  changes  induced,  but  are  essen- 
tially the  same  as  in  malignant  endocarditis — i.  e.,  rigors,  inter- 
mittent fever,  sweatings,  and  splenic  enlargement.  If  an  abscess 
of  the  myocardium  breaks  into  the  blood-stream,  there  are  in- 
farcts in  the  skin,  kidneys,  brain,  or  other  organs,  or  in  event 
of  rupture  of  the  heart-wall,  collapse  and  death.  The  clinical 
picture  is  usually  such  as  to  direct  attention  to  the  heart  as  the 
seat  of  the  disorder.  Yet  in  cases  of  diffuse  myocarditis  like  that 
narrated  by  Freund,  symptoms  referable  to  the  heart  may  be 
few  and  obscure,  wholly  out  of  proportion  to  the  gravity  of  the 
malady. 

Physical  Signs. — Inspection. — Pallor  is  said  to  be  conspicu- 
ous, and,  associated  with  either  apathy  or  restlessness,  is  very 
suggestive. 

Falpaiion. — The  pulse  is  weak,  empty,  and  strikingly  unsta- 
ble, and  the  cardiac  impulse  is  feeble  or  absent.  In  some  instances 
the  liver  and  spleen  may  be  palpable. 

Percussion. — This  may  or  may  not  disclose  an  increase  in 
the  area  of  deep-seated  cardiac  dulness,  but  if  such  increase  is 
associated  with  the  characters  of  the  pulse  just  mentioned,  it 
•  greatly  strengthens  the  diagnosis. 

Auscultation. — As  a  general  tiling  tlic  ear  detects  no  more 
than  enfeeblement  and  perhaps  muftting  of  the  heart-sounds. 
IMurmurs  are  present  only  when  dilatation  leads  tO'  muscular 
valvuhir  incompetence  or  endocarditis  or  pericarditis  is  associated. 

Diagnosis. — Unfortunately  the  diagnosis  of  acute  myocar- 
ditis is  usually  a  matter  of  conjecture,  and  reliance  must  be  placed 
on  the  history  of  some  infection  that  may  act  as  an  etiological 
factor,  even  more  than  on  the  symptoms  and  physical  findings. 
During  the  height  of  an  acute  infection,  as  diphtheria,  acute  rheu- 
marthritis,  and  typhoid  fever,  it  may  be  utterly  impossible  to 
diagnosticate  with  certainty  the  existence  of  acute  myocarditis, 
whereas  the  occurrence  of  the  physical  signs  described  during 
convalescence  renders  the  presence  of  the  disease  highly  probable. 
If  in  a  case  of  stispected  myocarditis  phenomena  of  sepsis  are 
observed,  they  point  strongly  to  a  suppurative  process. 


ACUTE  ^MYOCARDITIS  515 

Prognosis. — It  goes  without  saying  that  the  prognosis  is 
always  grave,  even  in  simple  myocarditis,  and  in  the  purulent 
form  is  absolutely  unfavourable.  Although  there  is  post-mortem 
evidence  that  small,  scattered  abscesses  in  the  heart-wall  some- 
times undergo  a  process  of  cure,  still  a  case  that  is  sufficiently 
outspoken  to  be  clinically  recognisable  is  from  its  nature  incura- 
ble. In  acute  interstitial  myocarditis  of  diphtheria  Komberg 
computes  the  fatal  termination  as  taking  place  in  about  one-third 
of  the  recognised  cases. 

It  is  not  unlikely  that  in  rheumatism  the  percentage  of  recov- 
ery is  larger.  This  would  appear  reasonable  when  we  consider 
that  the  parenchymatous  degeneration  is  not  so  intense  as  in 
diphtheria.  Although  all  cases  do  not  die,  yet  the  possibility  of 
sudden  death  should  never  be  forgotten;  and,  moreover,  this  pos- 
sibility is  not  wanting  in  any  given  case  simply  because  the  evi- 
dence of  cardiac  mischief  is  slight.  It  is  often  precisely  in  this 
class  of  cases  that  danger  is  most  imminent,  since  the  physician, 
patient,  and  friends  are  likely  to  be  thrown  off  their  guard,  and 
hence  permit  or  commit  indiscreet  effort. 

When,  on  the  other  hand,  symptoms  of  collapse  appear,  the 
danger  of  death  is  very  imminent.  Increasing  acceleration  of  the 
pulse  and  marked  instability,  the  heart  evincing  a  degree. of  fee- 
bleness out  of  all  proportion  to  the  demand  made  upon  it,  are 
signs  of  great  danger.  So  also  is  abnormal  retardation  of  the 
pulse-rate,  as  is  exceptionally  observed.  Delirium  renders  the 
prognosis  more  grave ;  and  the  occurrence  of  emboli  is  an  exceed- 
ingly bad  omen,  since  we  cannot  predict  how  many  are  likely  to 
follow  or  where  they  will  lodge.  Favourable  indications  are  to 
be  found  in  a  gradual  return  of  strength,  volume,  and  regularity 
to  the  pulse. 

Treatment. — We  possess  no  means  of  directly  influencing 
the  inflammatory  process  after  it  has  attacked  the  myocardium, 
and  therefore  our  efforts  must,  in  the  first  place,  be  directed  to 
the  prevention  of  myocarditis,  if  possible,  and  secondly,  to  pro- 
tecting the  heart-wall  from  all  extraneous  influences  which  can 
intensify  the  damage  it  is  sustaining  from  the  inflammation.  To 
the  former  end  is  the  early  employment  of  such  measures  as  may 
lessen  the  activity  of  the  primary  disease,  which  in  diphtheria 
involves  the  earliest  possible  use  of  the  antitoxine.     The  harm 


516  DISEASES   OF   THE   HEART 

tluit  may  result  from  delay  in  the  eiiiployiuent  of  this  remedy 
becomes  at  once  apparent  when  we  rcHect  on  liomberg's  statement 
that  the  symjjtoms  of  acute  myocarditis  may  arise  at  a  time  sub- 
sequent to  the  administration  of  diphtheria  antitoxine,  which  goes 
to  prove  that  the  longer  the  infection  is  at  work  in  the  system 
the  greater  the  likelihood  of  the  heart-muscle  becoming  affected. 
In  streptococcus  infection  the  antistreptococcic  serum  would  cer- 
tainly be  indicated ;  but  in  scarlatina,  typhoid  fever,  and  rheu- 
matism we  have  no  specific  remedy,  unless  with  the  exception  of 
salicylic  acid  in  rheumatic  fever ;  and  hence  we  must  endeavour 
to  promote  elimination  through  the  kidneys  by  administering 
copious  and  frequent  draughts  of  water,  and  subcutaneous  and 
rectal  injections  of  physiological  salt  solution. 

So  soon  as  symptoms  of  myocarditis  are  detected  the  indica- 
tion is  to  maintain  the  patient  in  absolute  repose  of  mind  and 
body.  Physical  effort  is  dangerous,  and  so  long  as  cardiac  weak- 
ness exists  the  patient  must  remain  in  bed.  lie  should  receive 
as  much  highly  nutritious  and  simple  food  as  he  can  assimilate — 
milk,  eggs,  broths,  etc.  The  bowels  are  to  be  kept  active,  though 
depleting  purgatives  are  to  be  avoided.  Strychnine  is  highly  ser- 
viceable, and  should  alcoholic  stinndants  or  ammonia  be  thought 
indicated,  they  are  to  be  administered. 

The  character  of  the  pulse  would  appear  to  call  for  digitalis, 
strophanthus,  etc.,  but  if  prescribed,  it  should  be  cautiously  and 
tentatively,  for  we  are  not  in  position  to  predicate  how  much  of 
the  myocardium  is  left  uninjured  and  capable  of  responding,  or 
whether  damage  may  not  accrue  to  fibres  that  have  imdergone 
extensive  degeneration.  Prsecordial  pain  and  restlessness  are  to 
be  allayed,  and  for  this  purpose  there  is  nothing  better  than  mor- 
phine. 

In  conclusion,  it  may  Ix'  rejH'ated  that  the  agencies  of  greatest 
service  are  rest,  food,  strychnine,  and  stimulants,  in  the  order 
mentioned.  In  diphtheria  it  is  often  perilous  to  allow  the  patient 
to  even  rise  up  in  bed  to  take  a  drink  or  to  evacuate  bladder  or 
rectum  ;  he  must  hv  kept  as  motionless  as  ])ossil)le.  Moreover,  it 
will  often  be  necessary  to  retain  the  ])atient  in  bed  for  many  weeks 
or  months.  A  rigid  enforcement  of  this  rule,  even  though  it  seems 
liard  and  cruel,  is  in  fact  a  disjday  of  greatest  kindness.  When  at 
length  such  a  measure  of  improvement  has  been  reached  that  abao- 


ACUTE  'MYOCARDITIS  517 

lute  rest  is  no  longer  needful,  the  patient  is  to  resume  exercise 
by  degrees,  and  at  first  with  the  utmost  caution.  Under  no  cir- 
cumstances is  an  attempt  to  ascend  stairs  to  be  permitted  before 
weeks  perhaps  of  gentle  moving  about  the  bed-chamber  have 
proved  that  the  heart  is  no  longer  unduly  taxed  by  such  efforts. 
During  this  period  of  convalescence  cautious  attempts  may  be 
made  to  strengthen  the  heart  by  resistance  exercises  and  saline 
baths.  At  this  time  benefit  may  be  derived  from  iron,  arsenic, 
and  other  ha?matics  and  nerve  tonics.  It  is  needless  to  add  that 
in  the  case  of  young  children  it  is  often  most  difficult,  yet  no  less 
important,  to  enforce  the  quiet  and  other  measures  necessary. 


CHAPTER    XX 
CHRONIC    MYOCARDITIS 

SYN.:  FATTY  DEGENERATION— FIBROID  DEGENERATION— 
MYOFIBROSIS  — WEAKENED  HEART— CHRONIC  CARDIAC 
INADEQUACY 

By  far  the  largest  number  of  persons  who  at  or  after  middle 
age  begin  to  manifest  signs  of  cardio-vascnlar  disturbance  are  not 
victims  of  valvular  disease.  Clinically  they  present  evidence  of 
failing  circulation  with  enlargement  of  the  heart  (In'pertrophy 
with  dilatation),  and  with  more  or  less  thickening  of  the  arteries. 
In  some  instances  certain  symptoms,  as  angina  pectoris,  point 
unmistakably  to  coronary  sclerosis,  with  its  consequent  alteration 
of  myocardial  nutrition,  but  for  the  most  part  there  is  nothing 
that  serves  as  a  criterion  of  the  nature  and  extent  of  the  change 
in  the  heart-muscle.  The  microscope  has  revealed  not  only  a  con- 
siderable variety  of  pathological  changes  in  these  cases,  but  also 
a  want  of  uniformity  or  constancy  in  the  relation  of  these  to  the 
symptoms.  In  other  words,  various  myocardial  alterations  seem 
capable  of  producing  the  same  clinical  picture,  and  conversely, 
various  clinical  pictures  appear  to  result  from  one  and  the  same 
pathological  change.  There  is  consequently  much  confusion  and 
uncertainty  still  regarding  the  patliogenesis  and  precise  relation- 
ship of  the  pathological  findings,  so  that  in  dealing  with  this  phase 
of  cardiac  disease  one  is  at  a  loss  whether  to  attempt  to  consider  it 
from  the  standpoint  of  the  pathologist  or  of  the  clinician.  In 
either  case  one  is  pretty  sure  to  get  himself  into  trouble.  German 
writers,  as  Romberg  and  Rosenbach,  group  the  cases  under  the 
head  of  Chronic  Cardiac  Insufficiency.  The  latter  maintains  that 
as  the  various  changes  in  the  heart-muscle  are  but  different  mani- 
festations of  one  process,  it  is  impossible  to  diagnosticate  anything 
more  than  heart-weakness,  while  Romberg  classifies  the  cases  ac- 
cording to  their  etiological  factors.  Thus  he  considers  in  one 
518 


CHRONIC  MYOCARDITIS  519 

group  those  due  to  coronary  disease,  those  to  obesity,  those  to 
strain,  and  those  to  nephritis,  those  to  excessive  consumption  of 
beer,  etc.  Such  a  division  is  in  accord  with  the  uncertainty  of 
our  knowledge  on  many  points,  and  also  has  the  merit  of  sim- 
plicity, but  it  is  open  to  the  objection  that  we  cannot  always  be 
sure  of  the  exact  etiology  of  all  cases  or  of  the  precise  mode  of 
operation  of  supposed  causes.  It  also,  as  he  himself  admits, 
necessitates  much  repetition,  and  therefore  I  have  decided  to  deal 
with  these  cases  under  the  heading  given  to  this  chapter.  I  am 
well  aware  of  the  objections  to  such  a  grouping,  and  know  that 
many  times  it  seems  simpler,  and  non-committal  in  a  sense,  to 
diagnose  them  according  to  the  gross  clinical  findings  of  hyper- 
trophy or  dilatation  or  idiopathic  enlargement  of  the  heart.  Still 
in  most  cases  the  microscope  shows  more  or  less  myocardial  de- 
generation, and  therefore  I  prefer  the  term  Chronic  Myocarditis. 

Morbid  Anatomy. — Under  chronic  myocarditis  the  ana- 
tomical conditions  usually  considered  are  those  of  fibrosis  and 
fatty  degeneration.  Conditions  interfering  with  the  nutrition 
of  the  heart  may  produce  either  or  both  of  these  changes,  or  the 
fibroid  may  be  dependent  on  the  fatty  change. 

Fibroid  degeneration  of  the  heart-muscle,  or  chronic  intersti- 
tial myocarditis,  may  represent  the  final  or  reparative  stage  of  the 
various  acute  forms  of  the  disease.  It  is  then  to  be  regarded  as  a 
conservative  rather  than  as  a  pathologic  process.  Thus  in  the 
case  of  infarction  of  the  heart,  or  myomalacia  cordis,  the  necrotic 
area  is  invaded  by  young  connective-tissue  elements,  which  finally 
are  metamorphosed  into  a  firm  fibroid  cicatrix.  Such  areas  of 
fibrosis,  or  scleroses,  are  large  or  small  according  to  the  size  of  the 
original  lesion.  Very  large  areas  are  rarely  found,  as  the  acute 
disease  would  have  probably  proved  fatal.  Except  by  the  forma- 
tion of  other  infarcts  this  process  does  not  tend  to  progress.  It  is 
only  when  the  occlusion  of  many  small  arteries  has  produced  mul- 
tiple scleroses  that  the  function  of  the  heart  is  impaired. 

Extreme  fatty  or  parenchymatous  degeneration,  leading  to  de- 
struction of  the  muscle  tissue,  may  be  the  cause  of  a  progressive 
fibrosis  of  the  myocardium.  Often  the  destructive  process  preced- 
ing the  interstitial  increase  is  a  coagulation  necrosis.  As  a  rule 
this  process  is  not  strictly  diffuse,  and  the  appearance  on  section 
is  of  numerous  scattered  streaks  and  spots  of  a  grayish  or  whitish 


520  DISEASES  OP  THE  HEART 

colour,  which  project  slightly  above  the  plane  of  the  section.  In- 
terstitial increase  is  not  always  dependent  on  antecedent  degen- 
eration, but  progressive  atrophy  of  the  muscle  and  increase  of 
the  fibrous  interstitial  tissue  may  occur  pari  passu  in  such  a  way 
as  to  render  it  difficult  to  determine  which  is  the  primary  and 
which  the  secondary  process.  In  this  case  the  fibrosis  is  more 
evenly  distributed  than  in  either  of  the  above  cases. 

Scleroses  are  most  frequently  observed  in  the  wall  of  the  left 
ventricle,  near  the  apex,  and  (m  the  posterior  side  in  the  upper 
two  thirds,  near  the  auricle,  in  the  papillary  muscles  of  the  left 
side,  and  in  the  interventricular  Sieptum.  The  fibrous  increase 
nuiy  cause  a  thickening  of  the  wall  of  the  heart — connective-tissue 
hypertrophy — or  the  presence  of  the  connective-tissue  elements 
may  so  reduce  the  tone  of  the  wall  as  to  cause  it  to  yield  to  the 
intracardiac  pressure  with  the  formation  of  bulgings,  the  so- 
called  partial  cardiac  aneurysm,  or  in  extreme  cases  with  rupture 
of  the  heart. 

Fatty  degeneration  is  manifested  by  a  general  paleness  with 
streaks  and  patches  of  a  yellowish-brown  colour.  The  markings 
of  such  a  heart  have  been  compared  to  those  of  a  faded  leaf.  The 
muscle  is  softer  than  normal  and  easily  torn.  Fatty  degeneration 
is  most  common  in  the  wall  of  the  left  ventricle  near  the  apex, 
next  in  the  right  ventricle,  the  interventricular  Sicptum,  and  the 
right  and  left  auricles  in  the  order  given.  It  usually  affects  the 
muscle  close  beneath  the  endocardium  more  than  that  near  the 
pericardium,  and  the  brownish  or  yellowish  mottling  is  sometimes 
plainly  observable  from  within  the  heart.  Microscopically  the 
protoplasm  of  the  fibres  is  seen  to  be  replaced  to  a  greater  or 
less  extent  by  fat  droplets.  These  are  arranged  in  rows,  and  are 
said  to  be  situated  at  the  junction  of  the  cross  and  longitudinal 
striations.  Very  advanced  fatty  degeneration  leads  to  a  disinte- 
gration of  the  fibres,  and  their  consequent  replacement  by  fibrous 
tissue. 

Fatty  overgrowth  consists  in  an  increase  of  the  normal  subepi- 
cardial layer  of  adipose  tissue.  This  is  normally  noticeable  only 
along  the  course  of  the  large  vessels,  but  in  well-marked  cases  of 
fatty  overgrowth  the  fat  covers  the  entire  organ  and  no  muscle 
is  to  be  seen.  A  thick  1)liiiikc(  of  fat  over  the  heart  acts  as  an 
effectual  impediment  to  its  work,  but  it  is  in  the  nature  of  an  out- 


CHRONIC   MYOCARDITIS  521 

side  force,  and  not,  as  is  the  case  in  fatty  degeneration,  a  disease 
of  the  muscle  itself.  Sometimes,  however,  the  adipose  tissue 
invades  the  subjacent  myocardium,  first  penetrating  between  the 
fibres  and  later  causing  the  complete  atrophy  and  disappearance 
of  the  muscle  elements.  This  process  may  penetrate  the  entire 
thickness  of  a  ventricular  wall,  and  of  course  greatly  impairs  its 
functionating  power. 

The  senile  heart  presents  a  varying  picture  made  up  of  ele- 
ments from  all  of  these  conditions.  As  a  rule  the  failing  nutri- 
tion of  old  age  induces  a  mixture  of  fibrous  and  fatty  degenera- 
tion. Fatty  overgrowth  is  common  in  those  elderly  persons  who 
incline  to  obesity.  The  senile  heart  may  be  hypertrophied — this 
when  associated  with  chronic  nephritis  and  general  arteriosclero- 
sis— or  atrophied  in  consequence  of  malnutrition  and  inaction. 
Very  frequently  this  atrophy  is  combined  with  the  condition  of 
autochthonous  pigmentation  already  described.  This  condition 
of  brown  atrophy  is  almost  characteristic  of  the  senile  heart. 

The  nutritional  disturbance  which  is  accountable  for  these 
degenerations  is  frequently  the  result  of  the  gradual  narrowing 
or  occlusion  of  the  coronary  arteries  or  their  branches.  This  may 
be  due  to  a  sclerosis  that  is  part  of  a  general  disease  of  all  the 
arteries,  or  it  may  be  due  to  obliterating  endarteritis  or  to  a  local 
atheroma  of  the  coronaries  either  at  their  orifices  or  branches. 
This  local  process  is  more  apt  to  take  place  in  the  descending 
branch  of  the  left  coronary  artery,  and  this  accounts  for  the  spe- 
cial predisposition  of  the  apical  portion  of  the  left  ventricular 
wall  to  fatty  and  fibroid  degeneration. 

Thrombosis  or  embolism  of  the  coronaries  induces  the  condi- 
tion of  myomalacia  cordis  already  considered.  The  walls  of  the 
arteries  may  become  of  bony  hardness,  or  atheromatous  in  patches. 
The  terminal  branches  may  be  converted  into  fibrous  cords  im- 
pervious to  the  circulating  fluid.  If  the  obliteration  of  one  artery 
takes  place  gradually  the  circulation  may  be  established  through 
branches  of  the  other.  The  reduction  of  the  blood-supply  to  the 
parts  affected,  and  especially  the  lack  of  oxygen,  indr.ces  fatty 
degeneration,  and  often  subsequent  fibrosis.  The  heart-muscle, 
probably  on  account  of  its  constant  activity,  feels  immediately 
any  lack  of  oxygen,  and  hence  the  myocardium  is  especially  prone 
to  fatty  degeneration. 
35 


522  DISEASES  OF  THE   HEART 

Changes  in  the  myocardinm  are  ahnost  always  found  associ- 
ated with  the  various  valvular  lesions,  and  with  hypertrophy  and 
dilatation  of  the  heart  from  any  cause. 

Etiology. — The  changes  of  the  heart-muscle  which  I  have 
chosen  to  group  under  the  generic  term  of  chronic  myocarditis 
are  of  slow  development,  and  presuppose  the  protracted  working 
of  influences  injurious  to  the  function  of  the  organ.  These  influ- 
ences are  for  the  most  part  conditions  which  cause  a  dispropor- 
tion between  the  demands  made  on  the  heart  and  its  nutritive 
supply — in  other  words,  which  require  the  heart  to  work  in  ex- 
cess of  its  nutrition.  The  influences  which  put  an  abnormal 
demand  on  the  heart  may  reside  within  the  organism  or  may  come 
from  without,  or  there  may  be  a  iniion  of  both. 

Under  the  first  head  are  degenerative  changes  of  the  vascular 
coats  and  chronic  kidney  diseases,  conditions  which  persistently 
augment  peripheral  resistance.  Conditions  residing  outside  the 
body  are  those  which  produce  long-continued  overstrain,  as  manual 
toil,  the  hardships  of  the  soldier's  or  the  sailor's  life,  the  toilsome 
daily  exertions  of  the  mountaineer,  excessive  consumption  of  beer, 
etc.  In  many  instances  influences  from  within  and  without  are 
conjoined.  Something  more  is  required,  however,  than  mere  in- 
crease of  work,  and  this  is  to  be  found  in  disorders  of  cardiac  nu- 
trition. The  blood  itself  may  be  of  poor  quality,  or  it  may  be  viti- 
ated by  toxines  of  one  kind  or  another,  or  the  blood  remaining 
healthy,  its  supply  to  the  heart  may  be  curtailed.  It  is  in  the  first 
way  that  fatty  degeneration  of  the  heart  is  brought  about  by  wast- 
ing diseases,  cancer,  chronic  suppurations,  repeated  loss  of  blood, 
secondary  and  pernicious  auirmia,  exhausting  discharges,  as 
chronic  diarrhcea,  by  insuflicient  food,  etc.  The  blood  may  be 
vitiated  by  the  toxines  of  acute  infectious  diseases,  by  chemical 
poisons,  and  prol^ably  by  toxic  substances  developed  within  the 
gastro-intestinal  tract,  some  of  them  of  bacterial  and  some  of  pu- 
trefactive origin.  Typlioid  and  scarlet  fever,  diplitheria,  acute 
rheumatism,  and  iiiflncii/a  ai'c  all  (•a|)able  of  setting  U]i  not  only 
acute  myocarditis,  but  chronic  niyocanlial  changes  of  an  allied  if 
not  identical,  yet  of  a  more  slowly  acting  nature.  Phosphorus, 
arsenical  poisoning,  and  alcohol  are  well-recognised  causes  of  fatty 
degeneration  of  the  heart. 

The  myocardial  degeneration  of  chronic  kidney  disease  may 


CHRONIC   MYOCARDITIS  523 

be  diiG  in  part,  at  least,  to  chronic  toxa-mia  acting  in  conjunc- 
tion with  prolonged  high  arterial  tension.  The  degenerations  de- 
pending upon  coronary  sclerosis  are  instances  of  the  third  kind — 
i.  e.,  of  defective  blood-su23ply. 

When  the  two  great  factors,  work  and  excessive  or  deficient 
nutrition  out  of  proportion  to  that  required  for  the  work,  are 
combined,  then  we  not  onl}^  have  myocardial  degeneration,  but  in 
time  also  inevitable  cardiac  inadequacy. 

The  hypertrophy  which  so  often  develops  in  association  with 
chronic  myocarditis  is  the  expression  of  an  attempt  at  compensa- 
tion. It  probably  evinces  an  effort  on  the  part  of  ISTature  to  repair 
the  damages  going  on  in  the  heart,  but  it  also  results  from  the 
necessity  on  the  part  of  this  organ  to  overcome  peripheral  re- 
sistance. 

Fraentzel's  idiopathic  enlargement  of  the  heart  was  thought 
by  him  to  result  from  the  consumption  of  an  amount  of  food  in 
excess  of  the  requirements  of  the  organism  and  of  the  individual's 
bodily  exercise.  Hence  it  is  found  in  its  most  typical  form  in 
persons  who  are  large  eaters,  and  who,  in  consequence  of  their 
particular  line  of  work,  are  compelled  to  be  sedentary.  Accord- 
ing to  Rosenbach,  physical  inactivity  is  an  important  element  in 
this  class  of  cases.  When  these  individuals  reach  middle  age 
they  are  usually  found  to  have  developed  corpulent  abdomens,  and 
they  generally  continue  to  increase  in  weight.  In  many  at  this 
time  the  previously  existing  high-pulse  tension  is  still  further  aug- 
mented by  degeneration  of  the  blood-vessels  and  kidneys,  often 
also  of  the  liver,  which  retrograde  changes  are  probably  to  be 
referred  to  the  same  etiological  factors.  So  long  as  cardiac  hyper- 
trophy enables  the  organ  to  meet  its  demands  its  functional  in- 
tegrity is  intact.  At  length,  however,  either  because  its  nutrition 
has  suffered  to  such  an  extent  that  it  cannot  meet  the  ordinary 
demands  made  upon  it,  or  because  extraordinary  work  is  sud- 
denly required,  as  from  some  undue  physical  effort,  the  heart 
finds  itself  overpowered,  and  symptoms  of  myocardial  incompe- 
tence set  in. 

In  the  working  classes,  in  soldiers,  in  sailors,  and  mountain- 
eers, in  persons  addicted  to  the  abuse  of  beer  and  other  alcoholic 
beverages,  who  at  the  same  time  perform  manual  toil,  influences 
of  various  kinds  are  active.    Food  defective  in  quality  or  quantity, 


524  DISEASES  OF  THE  HEART 

privations  and  hardships,  and  toxic  agencies  serve  to  intensify  the 
injurious  effects  of  overstrain.  In  southern  Germany,  notably 
Munich,  hypertrophy  and  degeneration  of  the  heart  in  its  most, 
typical  form  are  attributed  to  the  excessive  consumption  of  beer. 
Some  have  thought  this  due  to  the  great  vascular  strain  incident 
to  the  daily  intake  of  many  litres  of  fluid,  but  Krehl,  Rosenbach, 
and  others  recognise  in  addition  the  etiological  influence  of  toil 
and  the  nutritive  elements  contained  in  the  beer  as  well  as  of  the 
strain  put  upon  the  circulatory  apparatus  by  the  consumption  of 
excessive  amounts  of  the  fluid.  In  soldiers  and  mountaineers  who 
carry  heavy  knapsacks  strapped  upon  their  shoulders,  and  thus 
loaded  perform  wearisome  marches  day  after  day,  Rosenbach 
thinks  cardiac  function  is  impaired  through  respiratory  embar- 
rassment occasioned  by  constriction  of  the  chest,  and  through  the 
necessity  of  overcoming  abnormal  peripheral  resistance.  Athletic 
sports,  as  well  as  coffee,  tobacco,  and  alcohol,  he  considers  injuri- 
ous only  in  the  abuse,  not  their  use. 

Myocardial  degeneration  from  coronary  sclerosis  is  an  expres- 
sion of  inadequate  blood-supply,  either  circumscribed  or  general; 
and  that  one  may  understand  the  diverse  appearances  encountered 
I  think  it  well  to  quote  in  a  general  way  Leyden's  views  of  the 
mode  of  production  of  the  changes  in  this  class  of  cases. 

He  divides  these  into  four  groups  in  accordance  Avith  the  de- 
gree of  coronary  changes  and  the  rapidity  with  which  blood- 
supply  to  the  heart-muscle  is  shut  off,  as  follows : 

(1)  The  coronary  arteries  present  more  or  less  evidence  of 
sclerosis,  but  are  still  able  to  supply  the  heart  with  sufficient  blood 
to  maintain  its  nutrition.  Degeneration  does  not  take  place,  and 
the  organ  performs  its  functions  without  symptoms  referable  to 
coronary  disease.  Death  results  from  an  intercurrent  affection, 
and  knowledge  of  any  alteration  of  the  coronary  vessels  is  but  the 
accidental  revelation  of  an  autopsy. 

(2)  One  of  the  coronary  arteries,  usually  the  anterior  de- 
scending branch  of  the  left,  which  has  become  thickened,  subse- 
quently undergoes  obstruction  by  t]irond)osis.  When  this  takes 
place  slowly,  or  when  the  circuhition  is  but  imperfectly  cut  off 
from  the  area  supplied  by  the  affected  vessel,  the  wall  of  the  heart 
within  this  space  undergoes  fatty  or  fibroid  degeneration.  If  the 
thrombosis,  on  the  other  hand,  suddenly  and  completely  deprives 


CHRONIC   MYOCARDITIS  525 

the  part  of  its  nutrition,  then  this  area  breaks  down  into  the 
"  myomalacia  cordis  "  of  Ziegler.  Occasionally  the  extravasation 
of  blood  into  this  softened  area  gives  it  an  appearance  of  a  hsem- 
orrhagic  infarct.  When  rupture  of  the  heart  occurs,  it  is  gener- 
ally within  such  a  spot  of  acute  softening. 

(3)  Sclerosis  of  the  coronary  arteries  is  general  and  has  come 
on  gradually,  giving  rise  to  correspondingly  gradual  changes  in 
the  heart — i.  e.,  fibroid  degeneration  either  circumscribed  or  gen- 
eral. When  this  chronic  or  fibrous  myocarditis  is  diffused,  the 
ventricular  walls  are  apt  to  be  thin  and  dilated,  whereas  circum- 
scribed areas  of  induration  are  frequently  associated  with  hyper- 
trophy. In  rare  instances  this  development  of  new  connective 
tissue  is  attended  with  atrophy  of  the  muscle-fibres,  and  the  organ 
shrinks  in  size  after  the  fashion  of  a  cirrhotic  kidney. 

(4)  In  this  group,  the  coronary  sclerosis,  although  essentially 
chronic,  has  been  hastened  and  intensified  from  time  to  time  by 
acute  exacerbations  of  the  process,  thrombosis,  etc.  The  changes 
in  the  heart  are  therefore  twofold;  areas  of  acute  softening 
and  fatty  degeneration  are  interspersed  among  those  of  chronic 
myocarditis.  This  group,  which  blends  the  second  and  third, 
therefore,  is  the  one  most  often  encountered  by  the  physician. 

The  causes  of  coronary  sclerosis  are  obscure,  but  are  probably 
those  of  arteriosclerosis  in  general.  That  age  is  of  influence  seems 
attested  by  the  fact  that  more  or  less  evidence  of  the  change  is 
found  post  mortem  in  persons  past  middle  age,  while  it  is  rare 
under  forty  and  wanting  in  children.  Some  families  seem  to  pre- 
sent a  remarkable  tendency  to  sclerosis  of  the  coronaries  and  con- 
sequent myocardial  disease.  This  has  led  to  the  suggestion  of  a 
possible  hereditary  influence  in  its  production.  Some  individuals 
appear  to  be  endowed  with  "  arterial  tissue  or  vital  rubber  of  poor 
quality,  which  cannot  be  explained  in  any  other  way,"  as  is  so 
aptly  expressed  by  Osier,  "  than  that  in  the  make-up  of  the  ma- 
chine bad  material  was  used  for  the  tubing."  In  my  experience 
individuals  who  display  this  tendency  to  early  sclerosis  usually 
manifest  distinct  gouty  diathesis.  They  may  be  said  to  be  suffer- 
ing for  the  sins  of  their  ancestors.  I  have  long  had  the  conviction 
that  in  some  families  the  heart  is  the  locus  minoris  resistentice, 
in  some  displaying  particular  vulnerability  to  the  rheumatic  poi- 
son, and  in  others  appearing  unable  to  withstand  the  wear  and 


526  DISEASES  OP  THE   HEART 

tear  of  modern  business  life.  Certainly  it  is  not  very  nncommon 
to  elicit  from  a  patient,  himself  suffering  with  myocardial  disease, 
a  history  of  a  parent,  usually  his  father,  and  one  or  more  of  his 
brothers  and  sisters  having  died  suddenly  of  heart-disease. 

I  have  in  mind  now  a  family  in  which  the  father  is  reported 
to  have  died  of  ''  ossification  of  the  heart,"  while  of  three  of  the 
seven  sons  one  had  attacks  of  angina  pectoris,  another  had  heart- 
disease,  developed  at  middle  age,  and  the  third  died  suddenly 
with  a  dilated  heart,  after  having  suffered  from  one  or  two  out- 
spoken anginal  paroxysms. 

Males  suffer  from  chronic  myocarditis  more  often  than  do 
females,  but  this  is  probably  owing  to  their  greater  exposure  to 
those  conditions  favouring  the  development  of  myocardial  incom- 
petence rather  than  to  any  inherent  tendency  residing  in  the  fact 
of  sex  alone.  Women  frecpiently  manifest  clinical  and  post-mor- 
tem evidence  of  cardiac  degeneration,  and  according  to  Rosen- 
bach,  it  is  particularly  those  who  bear  children  in  rapid  succes- 
sion, and  are  still  further  depleted  by  lactation  and  insufficient 
nourishment. 

The  immediate  causes  of  cardiac  incompetence  cannot  always 
be  ascertained.  It  not  infrequently  develops  as  a  direct  result  of 
heart-strain  through  indiscreet  physical  efforts ;  but  it  also  may 
appear  without  any  such  determining  factor,  and  is  then  the  end- 
act  of  all  those  factors  that  have  led  to  the  degeneration.  Worry, 
grief,  excessive  business  cares,  as  in  times  of  financial  stress,  and 
even  emotional  excitement  of  other  kinds,  may  not  only  occasion 
loss  of  power  in  hearts  already  the  seat  of  myocardial  disease,  but 
are  said  to  be  an  etiological  element  in  the  development  of  the 
muscle-disease  itself. 

The  cardiac  inadequacy  of  chronic  nephritis  is  generally  the 
result  of  the  organ's  inability  to  longer  withstand  the  excessive 
tension  in  the  vascular  system.  It  may  develop  slowly  or  may  be 
precipitated  by  some  extra  exertion  or  other  source  of  added  heart- 
strain. 

Symptoms. — The  cardiac  incompetence  of  myocardial  dis- 
ease disj[)hiy8  clinical  pictures  of  considerable  variety  in  detail,  yet 
which  possess  the  same  fundamental  characters.  It  may  be  seen 
as  Fraentzel's  Idiopathic  Enlargement  of  the  Heart,  as  the  Senile 
Heart  so  graphically  jwrtrayed  by  Balfour,  as  a  case  of  angina 


CHRONIC  MYOCARDITIS  527 

pectoris  from  coronary  sclerosis  in  nocturnal  attacks  of  dys- 
pnoia,  known  as  cardiac  astlinia,  and  in  connection  with  chronic 
nephritis  or  diabetes,  or  both,  and  occasionally  as  a  mitral  or 
aortic  regurgitation  due  to  relative  insufficiency  from  dilatation. 

Idiopathic  cardiac  enlargement  occurs  for  the  most  part  in 
middle-aged  men  of  powerful  physique,  who  are  intellectually 
active,  but  physically  inactive.  It  is  especially  frequent,  therefore, 
in  men  of  affairs,  as  merchants  and  railroad  magnates,  and  in 
professional  men,  as  lawyers  and  clergymen,  who,  in  addition  to 
sitting  for  long  hours  at  their  desks,  generally  consume  large 
amounts  of  food.  For  years  there  is  in  such  individuals  an  abnor- 
mally high  and  sustained  pulse-tension,  which  resulting,  perhaps 
in  part,  from  abnormal  blood-pressure  within  the  abdominal  cav- 
ity, increases  as  the  girth  of  the  waist  increases.  This  state  of 
things  is  borne  without  special  discomfort  until  the  man  gets  well 
along  in  his  forties,  or  has  even  passed  his  fiftieth  year.  Then 
he  begins  little  by  little  to  notice  he  does  not  breathe  quite  so  easily 
as  formerly  on  ascending  stairs,  walking  up  a  slight  hill,  or  hurry- 
ing to  catch  a  street-car.  At  times,  particularly  after  breakfast 
or  a  more  than  ordinarily  hearty  meal,  he  finds  that  walking  at 
his  accustomed  pace  is  attended  by  a  feeling  of  uneasiness,  ful- 
ness, or  even  dull  pain  in  the  region  of  the  heart.  As  the  weeks 
go  on  he  finds  these  two  symptoms  become  decidedly  annoying, 
and  instead  of  wholly  subsiding  after  he  sits  down  they  remain 
as  a  vague  sense  of  discomfort  in  the  chest.  He  also  perceives, 
perhaps,  that  the  old  exertion  or  some  excitement  incident  to  his 
occupation  produces  consciousness  of  his  heart's  action,  a  verita- 
ble though  not  violent  palpitation.  As  a  rule  this  last  symptom 
is  not  at  all  pronounced,  being  subordinate  to  the  breathlessness 
and  pra?cordial  fulness. 

By  the  time  things  have  reached  this  pass  he  concludes  to  con- 
sult his  j^hysician,  who  finds  a  strong,  usually  regular  pulse,  no 
cardiac  impulse,  an  apparently  normal  heart's  dulness,  and  clear 
heart-tones  without  murmur,  but  the  aortic  second  sound  decid- 
edly accentuated.  If  the  radial  arteries  are  not  noticeably  stiff, 
and  the  urine  is  negative,  the  real  nature  of  the  case  is  apt  to  be 
overlooked,  and  the  symptoms  are  attributed  to  the  man's  increas- 
ing weight.  He  is  told  to  exercise  more,  eat  rather  less,  and  not 
to  worry.     Perhaps  he  is  advised  to  go  to  some  springs,  where  he 


628  DISEASES  OF  THE  HEART 

can  drink  laxative  waters,  or  be  goes  thither  on  the  recommenda- 
tion of  some  friend.  At  first  the  waters  and  active  exercise  seem 
to  make  him  feel  better,  but  after  returning  home,  and  having  re- 
sumed his  former  mode  of  life,  his  symptoms  reassert  themselves, 
this  time  in  greater  intensity.  He  again  seeks  his  physician,  who 
now  finds  the  pulse  is  accelerated,  the  heart  a  little  enlarged,  and 
the  liver  palpable.  The  urine  is  scantier  than  before, and  it  maybe 
contains  a  trace  of  albumin.  He  is  put  upon  digitalis  and  strych- 
nine, or  he  is  sent  to  Bad  Nauheim.  This  treatment  improves 
his  condition  to  a  greater  or  less  degree.  His  symptoms  are  less- 
ened or  disappear  entirely  for  a  number  of  months.  Then,  in 
consequence  of  return  to  his  old  ways  and  his  neglect  of  his  doc- 
tor's injunctions,  he  finds  his  enemy  has  again  attacked  him.  The 
former  course  of  treatments  is  repeated  with  less  brilliant  results. 
He  is  now  permanently  crippled,  but  is  still  able  to  attend  to  a 
l)art  of  his  duties.  As  months  go  on,  however,  his  shortness  of 
breath  and  other  symptoms  of  cardiac  inadequacy  grow  more  and 
more  pronounced,  therapeutic  measures  are  less  and  less  effective, 
and  at  length  this  once  powerful  and  active  man  of  affairs  is  laid 
by,  a  pronounced  suiferer  from  dyspna3a,  hepatic  stasis,  increasing 
(pdema,  scanty,  perhaps  albuminous  urine,  insomnia,  a  dull,  con- 
gestive headache,  cough,  and  frothy,  or  even  blood-tinged  sputum, 
a  feeble  and  often  arrhythmic  pulse,  a  dilated  and  feeble  heart — 
in  short,  all  the  signs  of  advanced  cardiac  insufficiency. 

In  other  cases  the  course  of  the  disease  from  initial  breathless- 
ness  to  complete  breakdown  of  heart-power  is  much  more  rapid. 
Instead  of  extending  over  two,  three,  or  more  years,  it  passes 
through  its  several  phases  in  a  few  months,  or  even  five  or  six 
weeks,  as  I  have  more  than  once  observed.  In  some  instances  the 
clinical  history  is  merely  that  of  ever-increasing  cardiac  debility, 
while  in  others  there  are  some  of  the  special  features,  as  cardiac 
asthma,  brady(;ardia,  or  even  the  so-called  Stokes-Adams  symp- 
toms, which  are  described  in  full  in  a  special  article.  Whatever 
the  variety  of  colouring,  the  general  picture  is  that  of  more  or 
less  rapidly  progressing  loss  of  heart-power,  and  the  ultimate  out- 
come is  always  the  same. 

Cases  of  chronic  myocarditis  are  conveniently  divided  into 
three  great  groups,  according  to  the  predominance  of  their  clin- 
ical manifestations.     These  are : 


CHROOTC  MYOCARDITIS  529 

(1)  The  arrhythmic  form,  in  which  the  pulse  is  strikingly 
irregular  and  intermittent,  now  slow  and  strong  for  a  few  beats, 
now  perhaps  rapid  and  feeble,  or  again  made  up  of  a  perfect  jum- 
ble of  large  and  small,  distinct  and  imperceptible,  slow,  rapid,  in- 
termittent waves  that  seem  to  fairly  tumble  over  each  other  in 
their  hurry,  or  to  lag  back  until  driven  hastily  onward  again  by 
the  impetuously  rushing  waves  behind.  In  a  word,  the  pulse  is  so 
lacking  in  regularity  of  rhythm,  force,  and  volume  tliat  to  count  it 
accurately  is  impossible. 

(2)  This  is  the  form  characterized  by  tachycardia  and  called 
the  tachycardial  form.  The  pulse  is  persistently  accelerated,  or 
in  a  few  instances  become  so,  in  paroxysms  which  so  annoy  or  even 
terrify  the  patient  that  he  comes  to  stand  in  mortal  dread  of  his 
attacks  of  palpitation. 

(3)  The  asthmatic  form,  distinguished  by  attacks  of  acute 
pulmonary  ttdema,  which  not  only  occasion  distress  and  terror  to 
the  patient,  but  throw  the  friends  into  a  state  of  scarcely  less 
alarm.  I  have  under  observation  at  the  present  writing  a  power- 
fully built,  active  business  man  of  sixty-three,  with  moderately 
stiff  arteries  and  a  hypertrophied  heart,  with  feeble  tones,  and  a 
scratching  systolic  murmur,  who  for  the  past  several  months  has 
lived  in  a  state  of  well-nigh  intolerable  nervousness  and  apprehen- 
sion. As  he  says,  he  has  completely  lost  his  nerve,  because  last 
September,  after  some  weeks  of  neglected  shortness  of  breath,  he 
was  one  evening  seized  with  an  attack  of  urgent  dyspnoea,  during 
which  the  pulse  was  scarcely  perceptible,  and  the  chest  emitted  a 
multitude  of  fine  crackling  sounds.  He  coughed  from  time  to 
time  and  expectorated  a  frothy  white  sputum.  The  attack  sub- 
sided after  the  hypodermic  administration  of  morphine  and  atro- 
pine. This  gentleman  has  had  one  recurrence  of  the  kind,  but  in 
the  meantime  has  scarcely  passed  a  week  without  hours  or  even 
days  during  which  his  heart  has  "  thumped  and  bumped,"  to  use 
his  expressive  words,  in  a  manner  which  throws  him  into  a  state 
of  great  alarm.  He  never  knows  when  this  palpitation  is  to 
occur,  but  it  seems  in  some  way  connected  with  temporary  aug- 
mentation of  pulse  tension.  It  is  also  quite  certain  to  folloAV 
excitement  over  business  affairs. 

The  pulse-rate  averages  from  88  to  95,  but  often  runs  up  to 
120  or  even  140,  and  such  is  the  throbbing  that  he  can  at  any 


530  DISEASES   OF  THE   HEART 

time  count  his  heart-beats  witlioiit  feeling  his  radial  pnlse.  There 
is  danger  of  death  during  his  attacks  and  he  knows  it,  whic^  of 
course  keeps  him  in  a  state  of  hourly  apj)rehension.  The  fore- 
going case  shows  the  occasional  blending  of  the  tachycardial  and 
asthmatic  types. 

Patients  of  the  arrhythmic  form  are  very  common  and  display 
the  greatest  tolerance  of  the  really  serious  cardiac  condition.  Thus 
I  knew  a  man  of  fifty-five  who,  notwithstanding  an  enormously 
dilated  heart  and  exceedingly  arrhythmic  pulse,  managed  to  drag 
on  for  nine  years  from  the  beginning  of  symptoms.  These  were 
not  very  severe;  panting  respiration  on  exercise,  a  feeling  of 
weakness,  so  that  he  could  not  attend  to  business,  and  consider- 
able fermentative  indigestion.  That  was  about  all,  and  at  last 
his  end  came  through  ascites  rather  than  distinctively'  cardiac 
inadetpuicy. 

It  must  not  be  supposed  that  cases  of  chronic  myocarditis  can 
always  be  clearly  separated  into  the  forms  just  described.  Many 
of  them  blend  the  symptoms  belonging  to  each  in  a  way  to  make 
a  very  complex  clinical  picture.  Neither  are  the  disturbances  of 
which  these  patients  complain  always  strictly  cardiac.  These  lat- 
ter may  be  said  to  be  dyspnrea,  heart-pain,  ])alpitation,  visceral 
congestions,  attacks  of  pulmonary  (fdema,  cough,  and  dropsy. 
They  are  all  present  in  varying  proportion,  not  perhaps  in  every 
case,  but  in  many  cases.  In  addition,  however,  there  are  very  sure 
to  be  numerous  other  complaints  which  in  all  likelihood  depend 
more  or  less  remotely  upon  the  disordered  circulation  and  per- 
verted visceral  function  arising  from  disordered  blood-flow.  Ver- 
tigo, insomnia,  neuralgias  and  myalgias,  nervousness,  irritability 
of  temper,  indefinite  sensations  in  the  region  of  the  heart,  numb- 
ness, and  formication — in  short,  a  score  of  sensations  which  the 
patient  connects  directly  willi  his  heart,  aiid  calls  on  the  medical 
attendant  to  explain  and  relieve.  They  are  a  large  part  of  the 
daily  plaint  of  these  chronic  sufferers  when  able  to  be  about  and 
in  a  state  of  partial  compensation.  When,  however,  really  serious 
symptoms  of  cardiac  insufficiency  set  in,  they  are  so  much  worse 
that  they  drive  away  more  trifling  sensations  and  dominate  the 
scene. 

All  cases  do  not  fall  distinctly  into  the  class  of  Idiopathic 
Cardiac  Enlargement  or  of  the  Senile  Heart,  but  occupy  a  sort  of 


CHRONIC  MYOCARDITIS  531 

intermediate  ground.  Nevertheless,  it  is  conducive  to  clearness 
to  try  to  classify  them,  as  is  essayed  to  do  in  this  chapter. 

The  senile  lieart  forms  but  a  part  of  a  general  degenerative 
process.  In  one  case  the  arteries  are  markedly  stiff  and  tortuous ; 
in  anutlior  tlio  urine  shows  evidence  of  pronounced  interstitial 
nephritis,  but  in  all  the  phenomena  of  cardiac  incompetence  domi- 
nate the  scene.  There  are  breathlessness  on  even  slight  exertion, 
feebleness,  digestive  disorders,  sensitiveness  to  cold  and  changes  of 
weather,  a  tendency  to  bronchitis,  and  insomnia.  In  some  there 
are  attacks  of  nocturnal  dyspnoea  of  greater  or  less  intensity,  flut- 
terings  of  the  heart,  vertigo,  or  even  syncopal  attacks. 

In  other  cases  the  breathing  assinnes  more  or  less  typically  the 
Cheyne-Stokes  type  (see  article  on  Cheyne-Stokes  Respiration), 
with  or  without  oedema,  pulmonary  congestions,  arrhythmic  feeble 
pulse,  and  the  usual  nuinifestations  of  progressing  asystolism. 

The  course  is  usually  slow,  the  symptoms  being  sometimes 
mild,  and  the  patient  cut  off  by  some  intercurrent  affection,  as 
senile  pneiunonia.  In  some  instances  there  is  history  of  attacks 
of  angina. pectoris  for  five,  ten,  or  even  twenty  years,  and  death 
at  last  is  sudden  and  unexpected.  There  are  other  cases,  chiefly 
men,  whose  cardiac  inadequacy  is  shown  by  acceleration  and 
arrhythmia  of  the  heart's  action,  inclination  to  cough  and  wheeze, 
and  various  so-called  gouty  manifestations  rather  than  by  pro- 
nounced dyspnoea  or  venous  stasis ;  the  so-called  arrhythmic  form. 
They  get  rather  breathless  on  exercise,  and  yet  then  can  walk  at  a 
moderate  rate  of  speed  without  much  difficulty.  They  have  times 
when  from  some  illness,  as  acute  bronchitis,  injudicious  strain  of 
one  kind  or  another,  they  are  laid  up  in  their  room  with  a  trace 
of  oedema  and  indications  of  failing  heart-power  that  look  very 
threatening,  and  yet  under  good  nursing  and  proper  medical 
attention  they  rally,  and  after  weeks  or  months  are  again  able  to 
be  about,  a  little  weaker  and  thinner,  a  little  more  breathless,  but 
on  the  whole  capable  of  getting  considerable  enjoyment  out  of 
their  quiet  existence. 

I  recall  an  old  gentleman  of  eighty  with  stiff  arteries,  urine  of 
poor  quality,  and  a  greatly  hypertrophied  heart,  the  first  sound 
accompanied  by  a  loud  systolic  basic  murmur,  the  aortic  second 
intensely  ringing,  who  yet  attended  daily  to  the  cares  of  a  large 
personal  property  besides  many  other  duties  of  a  public  and  pri- 


532  DISEASES  OP  THE  HEART 

vate  nature.  At  length  one  spring  he  and  his  friends  noticed  that 
he  began  to  breathe  with  difficulty  upon  ascending  stairs,  and  at 
rest  displayed  a  peculiar  sort  of  breathing  which  they  had  never 
observed  before.  Notwithstanding  this  difficulty  he  came  to  con- 
sult nie  at  my  office,  and  seemed  surprised  when  he  was  told  to 
return  home,  give  up  his  business,  and  remain  in  the  house.  His 
pulse  was  rather  unstable,  occasionally  intermittent,  but  not  nota- 
bly accelerated.  Ilis  respiration  was  only  moderately  dyspnoeic 
as  he  moved  about  the  room,  but  after  he  had  been  sitting  still 
for  some  time,  and  particularly  M'hen  asleep,  it  became  irregular, 
with  short  ])eriods  of  nearly  but  not  quite  complete  cessation  of 
breathing,  which  were  then  succeeded  by  gradually  deepening  in- 
spirations until  they  grew  full  and  vigorous.  They  then  died 
away  rapidly  into  apparent  apncea.  Close  observation  detected 
that  at  some  of  these  times  he  yet  breathed  faintly,  while  at  others 
he  breathed  not  at  all.  Some  of  the  dyspnoeic  periods  were 
longer  and  more  pronounced  than  others,  and  for  minutes  together 
others  of  them  presented  all  the  characters  of  typical  Cheyne- 
Stokes  respiration. 

During  these  periods  he  did  not  seem  subjectively  conscious  of 
distress.  Under  appropriate  treatment  of  a  stimulating  and  elimi- 
nating kind  and  prolonged  confinement  to  one  floor,  afterward  to 
the  house,  his  irregular  type  of  breathing  gradually  left,  the  heart 
grew  steadier  and  stronger  in  action,  and  he  came  to  look  upon 
himself  as  pretty  well.  He  required  rather  close  watching  to  pre- 
vent indiscretions,  chiefly  in  way  of  exercise,  but  as  time  went  on 
he  was  able  to  transact  a  little  business  and  to  enjoy  the  visits  of 
his  friends.  In  this  manner  this  gentleman  was  able  to  live  on 
for  two  years.  When  at  length  the  final  struggle  came,  it  was  in 
the  form  of  a  renewal  not  of  incomplete  Cheyne-Stokes  respira- 
tion, but  of  a  most  distressing  dyspnoea,  which  gave  him  no  peace 
even  when  (piict  in  bed.  It  was  not  attended  with  notable  signs 
of  cardiac  failure,  and  no  particular  evidence  of  renal  insuffi- 
ciency. It  may  have  been  due  to  bulbar  sclerosis ;  but  at  all 
events  it  at  length  necessitated  the  hypodermic  administration  of 
such  heroic  and  frequent  doses  of  morjihine,  that  he  at  last  ex- 
pired in  a  state  of  complete  narcosis. 

In  tlie  case  of  a  man  of  seventy-one,  wlio  had  been  a  well- 
known  journalist,  the  initial  symi)t,om  so  far  as  could  be  ascer- 


CHRONIC  MYOCARDITIS  583 

tallied  was  an  attack  of  dyspnoea,  which  seized  him  one  night  after 
he  had  retired.  He  fell  asleep,  and  after  a  few  minutes  sprang  up 
in  bed,  clutching  at  his  throat,  exclaiming  he  was  going  to  stran- 
gle. This  so  terrified  him  that  at  length  he  arose,  dressed,  and 
compelled  his  valet  to  keep  him  walking  up  and  down  in  the  gar- 
den for  the  remainder  of  the  night.  When  I  saw  him  the  follow- 
ing afternoon  he  was  still  greatly  agitated  and  suffering  from 
choking  spells.  A  hypodermic  of  an  -}  of  morphine,  with  atropine 
in  the  ordinary  combination,  gave  six  hours'  uninterrupted  sleep 
the  next  night,  although  during  his  repose  his  breathing  was  typi- 
cally Cheyne-Stokes.  This  patient's  pulse  was  very  arrhythmic, 
his  arteries  sclerotic,  his  heart  dilated,  with  a  blowing  apex-mur- 
mur and  feeble  sounds.  His  urine  was  that  of  a  moderate  renal 
cirrhosis,  and  he  suffered  from  prostatic  enlargement.  His  stom- 
ach was  dilated,  and  he  had  any  amount  of  flatulent  distention  of 
the  bowels.  Altogether  it  was  an  unpromising  case,  yet  persistent 
and  vigorous  treatment  with  cardiac  tonics  and  cathartics,  with  as 
strict  a  control  of  the  dietary  as  was  possible  with  an  irritable, 
self-willed  old  gentleman,  at  length  pulled  him  out  of  his  deplor- 
able condition.  For  four  years  he  was  an  invalid,  having  times 
of  profound  physical  and  mental  depression,  and  periods  of  grave 
cardio-vascular  disturbance,  during  which  oedema  more  than  once 
appeared.  These  periods  of  distress  were  alternated  with  seasons 
of  comparative  immunity  from  symptoms,  and  yet  they  were  in- 
terspersed with  numerous  attacks  of  bronchitis,  mild  ursemic 
manifestations,  and  once  an  acute  pleurisy  with  effusion  that  even- 
tually necessitated  paracentesis. 

More  than  once  he  rallied  from  what  it  seemed  must  prove  his 
final  illness  ;  and  thus  actually  kept  alive  by  cardiac  tonics,  he  man- 
aged to  drag  out  four  years  of  chronic  cardiac  inadequacy.  When 
at  length  his  end  came,  it  was  quite  sudden,  although  preceded 
by  days  of  more  than  usual  feebleness  that  had  confined  him  to 
his  bed.  Although  this  patient  displayed  marked  general  debility, 
with  slowly  increasing  cardiac  asthenia,  he  never  again  suffered 
to  any  extent  from  his  nocturnal  dyspnoea,  and  never  had  an  attack 
of  angina  pectoris.  He  frequently  complained  of  obstinate  chest 
pains,  but  these  were  unmistakably  an  intercostal  neuralgia,  as 
shown  by  numerous  hypersesthetic  areas. 

This  case  belonged  to  what  may  be  styled  the   arrhythmic 


534  DISEASES  OF  THE   HEART 

group,  in  which  the  cardiac  insufficiency  is  shown  by  such  an 
irregularity  and  intermittence  of  the  heart's  action  that  it  consti- 
tutes a  veritable  delirium  cordis. 

Radizewsky  has  shown,  conclusively  as  it  seems  to  me,  that 
when  the  pulse  displays  these  characters  there  is  extensive  fibroid 
degeneration,  chiefly  of  the  auricles,  which  both  clinically  and 
post  mortem  are  found  dilated.  In  his  communication  upon  the 
subject  he  quotes  Hampeln's  researches,  which  demonstrated  that 
perfect  regularity  of  the  pidse  is  frequently  seen  in  cases  in  which 
subsequent  necropsy  discloses  extensive  fatty  degeneration  of  the 
left  ventricle.  In  other  words,  the  state  of  the  ventricle  cannot 
be  determined  by  the  state  of  the  pulse.  Radizewsky's  findings 
have  always  seemed  to  me  to  explain  the  protracted  course  which 
so  often  characterizes  cases  in  which  the  pulse  is  strikingly 
arrhythmic. 

Degeneration  and  dilatation  of  the  auricles  impair  the  func- 
tional integrity  of  the  heart-muscle,  but  can  never  so  seriously 
threaten  life  as  when  the  wall  of  the  left  ventricle  is  degenerated. 
I  have  seen  many  of  these  cases  with  unmistakable  cardiac  inade- 
quacy drag  along  for  months  and  even  years  after  the  heart  had 
become  so  feeble  and  arrhythmic  that  it  seemed  impossible  for  it 
to  maintain  the  circulation. 

On  the  other  hand,  exi)erience  has  taught  me  to  dread  those 
degenerated  and  senile  hearts,  which  are  apparently  not  much 
dilated,  yet  give  rise  to  dyspna'a  of  effort,  while  the  pulse  remains 
accelerated,  but  perfectly  regular.  Sueli  hearts  are  usually  refrac- 
tory to  treatment,  and  are  apt  to  surprise  one  disagreeably  by 
stopping  suddenly  and  unexpectedly.  They  belong  to  the  tachy- 
cardial  form  of  chronic  myocarditis. 

In  my  experience  the  clinical  picture  of  the  senile  heart  is 
very  rarely  that  of  great  dropsy  and  extensive  visceral  congestion 
with  overdistention  of  the  cardiac  chambers,  as  in  the  terminal 
stage  of  Fraentzel's  Tdio])athic  Enlargement  of  the  Heart. 

In  the  heai't  with,  coronary  sclerosis  the  consequent  interfer- 
ence with  nutrition  of  the  heart-muscle  leads  to  changes  of  a 
chronic  nature  in  tlic  majority  of  cases.  In  others,  circulation 
within  the  coronarv  arteries  is  more  or  less  suddenly  shut  oif,  and 
the  heart-muscle  suffers  with  corresponding  acuteness. 

Consequently  the  symptoms  due  to  coronary  diseasQ  are  di- 


CHRONic  MYOCARDITIS  535 

verse,  and  are  best  divided,  as  by  Leyden,  into  acute,  subacute, 
and  chronic. 

In  the  acute  form  the  clinical  history  is  confined  to  a  few  days, 
hours,  or  even  minutes.  The  symptoms  are  due  to  coronary 
thrombosis  with  secondary  myocardial  softening,  to  sudden  rup- 
ture of  the  heart  in  some  area  of  insidious  fatty  degeneration,  or 
of  acute  molecular  necrosis  (myomalacia  cordis),  or  the  symptoms 
consist  only  of  a  sudden  diastolic  arrest  of  the  heart's  action. 

The  symptoms  of  Jieart-rujjhux  may  be  a  sudden  sharp  attack 
of  angina  pectoris  or  of  vague  pra^cordial  distress  and  oppression 
with  profound  prostration.  The  action  of  the  heart  is  feeble  and 
disordered,  and  the  organ  fails  to  respond  to  stimulants.  The  in- 
tellect is  generally  clear,  but  unconsciousness  may  be  present.  In 
some  cases  there  are  symptoms  of  gastric  disturbance,  even  vomit- 
ing, and  the  case  is  thought  to  be  one  of  gastric  disorder.  If  life  is 
prolonged  for  several  days,  as  very  rarely  happens,  the  first  vio- 
lence of  the  attack  abates,  not  to  be  renewed,  or  the  angina  and 
pra^cordial  distress  recur  from  time  to  time  with  steadily  increas- 
ing asystolism  and  death.  In  other  cases  of  cardiac  rupture  the 
symptoms  are  chiefly  those  of  rapidly  failing  circulation  with 
insensibility  and  death  from  acute  pulmonary  oedema. 

With  the  onset  of  symptoms  the  nearest  physician  is  hastily 
summoned,  and  on  arriving  at  the  patient's  side  finds  him  mori- 
bund. Stimulants  prove  inert,  and  the  doctor  signs  the  death 
certificate  without  having  been  able  to  accurately  diagnose  the 
condition.  If  he  examines  the  heart  he  discovers  clear  feeble 
sounds  without  any  appreciable  increase  in  the  area  of  dulness. 
In  other  cases  cardiac  dulness  is  increased,  but  unless  a  slow 
escape  of  blood  into  the  pericardium  produces  the  outline  charac- 
teristic of  pericardial  efi^usion,  the  augmentation  of  dulness  is 
attributed  to  dilatation,  and  a  diagnosis  is  made  of  paralysis  of 
the  heart  (acute  asystolism),  which  seems  borne  out  by  the  weak- 
ness of  the  sounds  and  strikingly  poor  quality  of  the  pulse.  In 
such  a  case  recently  narrated  to  me  death  supervened  in  half  an 
hour  from  supposed  acute  dilatation,  and  yet  the  sac  was  found 
absolutely  distended  with  blood. 

In  another  form  of  this  acute  type  of  coronary  sclerosis  the 
patient  appears  as  well  as  ordinary,  having  made  no  complaint 
that  led  to  a  suspicion  of  his  having  heart-disease,  and  yet  in  the 


536  DISEASES  OP   THE  HEART 

midst  of  his  activities,  while  at  work  in  his  office,  on  rising  from 
dinner,  etc.,  he  suddenly  falls  dead.  lie  may  turn  pale,  speak  of 
vertigo,  give  a  groan,  or  in  some  way  attract  the  attention  of  his 
family,  who  spring  to  catch  him  as  he  sinks  to  the  floor  in  fatal 
syncope.  The  mahogany  flushing  of  the  face  and  few  gasping  in- 
spirations suggest  death  from  apoplexy,  but  in  reality  it  is  from 
sudden  diastolic  arrest  of  the  heart.  In  such  instances  the  degen- 
erative process  has  invaded  some  of  the  vital  centres  in  the  heart, 
probably  in  the  upper  portion  of  the  interventricular  sssptum. 

In  cases  which,  according  to  Leyden's  classification,  may  be 
called  subacute,  there  are  attacks  of  angina  pectoris  extending 
over  a  period  of  weeks  or  months.  They  differ  much  in  difi"erent 
cases,  as  regards  severity  and  frequency  of  occurrence.  As  a  rule, 
however,  they  grow  more  intense  and  more  frequent.  The  suf- 
ferer speedily  becomes  incapacitated  for  business,  keeps  in  the 
house,  or  ventures  forth  only  on  mild,  still  days,  grows  daily 
weaker  and  paler,  and  is  very  apt  to  lose  flesh.  Death  comes  at  last 
either  from  slowly  increasing  asystolism,  or  suddenly  during  an 
anginal  paroxysm.  The  pulse  in  such  cases  is  usually  regular,  and 
but  moderately  if  at  all  accelerated,  while  examination  of  the  heart 
is  generally  negative.  The  arteries  may  display  some  stiffness, 
but  aside  from  the  patient's  age  and  his  attacks  of  pain  there  is 
little  to  indicate  chronic  myocarditis. 

Cases  coming  under  the  chronic  head  run  a  slow  course  and 
extend  over  years,  instead  of  months,  five,  ten,  or  even  twenty. 
The  individuals  are  always  conscious  of  their  liability  to  an 
attack,  and  hence  deport  themselves  most  circumspectly,  eating 
and  drinking  moderately,  walking  and  exercising  carefully,  avoid- 
ing raw  cold  winds,  and  shunning  excitement  tind  provocation 
to  anger,  lest  at  once  their  cn(>niy  he  upon  them.  Their  general 
health  does  not  suffer  greatly  at  first,  although  as  years  go  by 
they  look  and  act  like  invalids.  A  few  experience  some  shortness 
of  breath,  or  may  exceptionally  suffer  from  veritable  cardiac 
asthma.  As  a  rule,  however,  their  one  symptom  is  their  terrible 
angina.  Their  pulse  is  generally  regular,  always  appreciably 
tense,  and  their  hearts  are  negative  on  examination.  Deatli  comes 
through  intercurrent  disease  or  during  an  attack.  For  further 
particulars  the  reader  is  referred  to  the  chapter  on  Angina  Pec- 
toris. 


CHRONIC   MYOCARDITIS  537 

In  general  arteriosclerosis  there  are  often  symptoms  of  circu- 
latory failure  which  are  apt  to  be  attributed  to  cardiac  inadequacy 
alone,  when  in  reality  it  is  the  arterial  stiffness  that  is  responsible 
for  the  stasis  and  a'dema.  The  heart  may  in  such  be  atrophied 
or  of  normal  size,  but  as  a  rule  it  is  hypertrophied.  The  condi- 
tion of  the  myocardium  depends  upon  the  degree  of  its  nutrition 
with  relation  to  its  work,  and  as  the  aorta  and  coronaries  share  to 
a  greater  or  less  extent  in  the  sclerotic  process,  the  heart-muscle 
is  not  intact.  Xevertheless,  its  driving  power  is  often  adequate 
for  years  after  the  blood-vessels  have  become  rigid  and  beady. 
At  length  it  reaches  the  limit  of  its  compensatory  ability,  and  vas- 
cular resistance  still  augmenting,  the  heart-walls  begin  gradually 
to  yield  to  the  strain  of  maintaining  arterial  circulation,  and  dila- 
tation slowly  supersedes  hypertrophy. 

In  some  cases  injudicious  physical  effort,  suddenly  or  too  often 
exerted,  causes  acute  overstrain  of  the  already  too  greatly  taxed 
heart,  and  symptoms  of  cardiac  insufficiency  set  in  rapidly  instead 
of  slowly.  These  are  not  peculiar,  but  possess  the  ordinary  char- 
acters of  retarded  circulation,  breathlessness,  slight  a^dema  of  the 
ankles,  scanty,  perhaps  albuminous  urine,  pulmonary  and  hepatic 
congestion.  The  superficial  veins  stand  forth  still  more  promi- 
nently, the  rigid,  tortuous,  uneven  arteries  show  a  thready,  often 
flickering  pulse,  which  is  accelerated  and  often  irregular  both  in 
force  and  rhythm.  The  heart  is  found  more  or  less  increased  in 
size,  and  its  sounds  are  altered  in  quality  and  proper  relative 
intensity.  There  may  or  may  not  be  murmurs  at  apex  or  base 
indicative  of  atheromatous  changes  in  the  valves,  but  the  aortic 
second  tone  is  nearly  always  ringing  and  metallic. 

The  patient  loses  strength,  and  finally  takes  to  the  house  per- 
manently. Dyspnoea  grows  apace  and  not  infrequently  assumes 
the  characters  of  cardiac  asthma  or  of  Cheyne-Stokes  respiration. 
Urine  grows  still  scantier,  dropsy  advances,  orthopnoea  sets  in, 
troublesome  cough,  and  frothy,  blood-tinged  expectoration,  betoken 
ever-increasing  stasis  within  the  pulmonary  vessels,  and  the  pa- 
tient succumbs  after  weeks  or  months  to  general  exhaustion,  car- 
diac asthenia,  or  an  attack  of  acute  pulmonary  oedema. 

Chronicity  is  the  essential  feature  of  this  type  of  cardio-vascu- 

lar  inadequacy.     It  is  not  uncommon  for  cases  of  arteriosclerosis 

to  drag  on  for  several  years  under  the  picture  of  senility  and  gen- 
35* 


538  DISEASES  OF   THE   HEART 

eral  decrepitude,  and  deatli  to  come  at  last  as  a  result  of  acute 
bronchitis,  pneumonia,  or  even  of  renal  inadequacy. 

Exceptionally,  although  the  total  number  of  such  eases  is  not 
snuill,  the  termination  is  through  cerebral  thrombosis.  Rupture 
of  a  blood-vessel  in  the  brain  is  not  so  frequent  in  senile  arterio- 
sclerosis as  in  younger  persons  whose  renal  cirrhosis  leads  to  enor- 
mous left-ventricle  hypertrophy. 

Chronic  nephritis  leads  to  very  serious  changes  in  the  heart- 
muscle.  Clinically,  this  is  shown  by  hypertrophy  of  the  left  ven- 
tricle either  alone  or  as  a  part  of  a  general  cardiac  enlargement. 
The  myocardium  may  or  may  not  be  seriously  degenerated,  but 
whether  it  is  or  not,  it  is  subjected  to  an  enormous  peripheral 
resistance  to  successfully  cope  with  which  it  is  compelled  to  un- 
dergo hypertrophy.  I  do  not  intend  to  discuss  the  various  theories 
which  have  been  advanced  to  explain  this  increase ;  for  these  the 
reader  is  referred  to  works  dealing  with  kidney  diseases. 

The  pulse  of  chronic  nephritis  shows  prolonged  high  tension, 
which  is  primarily  of  renal,  not  cardiac,  origin.  If  the  kidney 
changes  are  of  slow  development,  as  in  chronic  interstitial  nephri- 
tis, or  if  the  patient  is  not  carried  off  by  the  sudden  onset  of  renal 
inadequacy,  there  surely  comes  a  time  when  the  heart,  struggling 
with  abnormally  high  endocardial  blood-pressure,  is  able  only 
with  difficulty  to  withstand  the  enormous  resistance  in  the  arterial 
system.  Then  gradually  or  suddenly,  according  to  circumstances, 
the  wall  of  the  left  ventricle  gives  way. 

If  slowly,  the  volume  of  urine  begins  to  fall  off,  and  the  patient 
finds  his  wonted  physical  efforts  are  attended  by  shortness  of 
breath  and  palpitation,  and  his  pulse-rate  is  found  to  be  decidedly 
augmented.  Signs  of  venous  congestion  and  pronounced  cardiac 
dilatation  are  usually  wanting  at  this  stage.  Unless  the  danger 
is  recognised  and  means  are  resorted  to  of  restoring  the  equilibri- 
um between  pulse-tension  and  heart-power,  cardiac  insufficiency 
grows  daily  more  apparent,  and  the  patient  is  at  length  compelled 
to  remain  inactive.  Examined  at  this  time,  he  is  found  to  evince 
unmistakable  signs  of  failing  circulation.  The  pulse  is  rapid  and 
perhaps  of  poor  quality ;  the  liver  is  palpable  and  more  or  less  ten- 
der; tension,  and  it  may  be  pitting  of  the  ankles,  is  detected;  the 
tongue  is  coated,  breath  foul,  and  the  urine  is  apt  to  be 'decidedly 
scanty  and  albuminous.     If  the  heart  is  examined,  the  apex  is 


CHRONlC   xMYOCARDITIS  539 

displaced  and  lacking  in  concentration  and  force,  the  second  sound 
at  the  right  of  the  sternum  is  somewha-t  enfeebled,  and  the  pul- 
monic is  nearly  or  quite  as  intense. 

The  striking  alteration  in  the  heart-findings  consists  in  the 
peculiar  reduplication  of  the  sounds  at  tlie  apex,  which  is  known 
as  gallop  rhythm  (see  introductory  chapter).  Occurring  in  the 
course  of  chronic  Bright's  disease  this  phenomenon  is  of  very  evil 
portent,  for  it  indicates  that  the  left  ventricle  is  yielding  to  the 
abnormal  strain  and  tottering  on  the  verge  of  an  irreparable 
breakdown.  In  most  cases  treatment  is  unavailing,  symptoms  of 
stasis  progress,  and  dyspnoea  becomes  most  distressing.  It  may 
be  of  the  C'heyne-Stokes  type,  but  is  more  often  of  a  paroxysmal 
nature,  coming  in  waves,  as  it  were,  with  evidences  of  great  agita- 
tion, even  alarm,  on  the  part  of  the  patient,  yet  without  corre- 
sponding signs  of  more  than  usual  cardiac  failure.  This  form 
of  dyspncea  is  probably  partly  of  toxic  (urtemic)  and  partly  of 
cardiac  origin.  jSTevertheless,  the  insufficiency  of  the  heart  aug- 
ments, renal  excretion  fails  correspondingly,  and  after  the  lapse 
of  weeks  or  a  few  months  the  patient  dies  with  ursemic  manifesta- 
tions or  from  acute  pulmonary  oedema. 

There  are  other  cases  of  Bright's  disease  in  which  cardiac  in- 
competence sets  in  abruptly.  This  is  usually  owing  to  some  indis- 
creet effort  or  excess  which  causes  rapid  dilatation  of  the  left  ven- 
tricle. The  symptoms  are  much  the  same  as  in  the  more  gradu- 
ally evolved  loss  of  compensation,  but  are  apt  to  be  of  far  greater 
intensity.  Examination  shows  feeble  apex-beat,  displaced  far  to 
the  left  and  perhaps  downward,  enormous  increase  of  cardiac 
dulness,  and  a  systolic  apex-murmur,  which  often  replaces  the  first 
sound,  and  a  feeble  second  tone  except  in  the  pulmonary  area, 
where  it  is  intensified.  The  liver  swells  rapidly,  is  often  painful 
and  very  tender,  particularly  in  the  epigastrium.  Dropsy  sets  in, 
extends  rapidly  upward,  and  invades  the  serous  cavities.  The  pa- 
tient suffers  from  orthopnoea  with  paroxysmal  exacerbations,  from 
severe,  tensive  headache,  insomnia,  or  it  may  be  somnolence,  and 
many  other  distressing  symptoms  of  combined  cardiac  and  renal 
inadequacy.  Few  clinical  pictures  are  more  distressing,  and  7ione 
are  more  hopeless. 

In  many  cases  in  which  there  are  enlarged  hearts  with  stiff- 
ened arteries  and  urinarv  findin2,'s  of  renal  sclerosis  it  is  difficult 


540  DISEASES  OF  THE   HEART 

to  say  whether  the  symptoms  of  failing  circulation  are  due  pri- 
marily to  incompetence  on  the  part  of  the  heart  or  of  the  kidneys. 
Some  of  these  patients  manifest  symptoms  of  slowly  failing  heart- 
power  for  many  months  before  being  compelled  to  regard  them- 
selves as  hopeless  invalids.  I  recall  one  gentleman  of  fifty-eight 
with  this  combination  of  cardio-vascnlar  and  renal  degeneration, 
who,  nearly  two  years  before  his  death,  suft'ered  from  paroxysms 
of  dyspnoea  which  becanse  of  his  rapid,  unsteady  pulse  was 
thought  cardiac,  but  seemed  to  me  in  reality  ura:^mic.  It  did  not 
yield  until  pulse-tension  was  reduced  by  frequent  doses  of  nitro- 
glycerin. Another  gentleman  of  forty-seven  with  the  same  asso- 
ciation of  diseases  used  to  complain  that  he  could  not  breathe 
"  more  than  an  inch  deep."  This  patient's  heart  manifested 
clinically  the  most  enormous  enlargement  I  have  ever  seen.  His 
breakdown  was  initiated  three  years  before  by  a  "  century  run  " 
on  his  bicycle. 

Diabetes  melliius  occurring  after  middle  age,  and  usually  con- 
joined with  vascular  and  renal  changes,  is  often  seriously  compli- 
cated by  symptoms  of  cardiac  incompetence.  The  arteries  are 
more  or  less  stiff,  the  heart  is  hypertrophied  and  dilated,  and  its 
action  is  rapid  or  ])ounding,  sometimes  intermittent.  Glycosuria 
is  the  feature  which  has  especially  to  be  combated,  and  yet  one 
must  never  lose  sight  of  the  cardio-vascular  symptoms.  At  the 
present  writing  I  have  under  observation  two  ladies  who  have  dia- 
betes mellitus  with  atheromatous  arteries  and  hypertrophied 
hearts.  In  one,  whose  age  is  not  far  from  seventy,  the  main  com- 
plaint (so  long  as  strict  diet  keeps  down  the  glycosuria)  is  of  great 
weakness,  palpitation,  and  shortness  of  breath  upon  exertion. 
The  other  patient,  of  about  sixty,  suffers  chictiy  from  dyspnoea, 
attacks  of  palpitation,  and  faintness.  On  two  occasions  in  the 
early  morning  hours  she  has  been  awakened  by  a  sense  of  suffoca- 
tion, and  has  nearly  died  from  acute  ])ulmonary  (rdema.  Signs 
of  cardiac  inadequacy  are  present  at  all  times,  and  yet  she  shows 
no  traces  of  dropsy  or  special  venous  congestion.  In  both  of  these 
cases  hypertrophy  still  predominates,  and  is  able  to  endure  the 
high  endocardial  blood-pressure  so  long  as  this  is  not  intensified  by 
the  strain  of  physical  effort.  The  nocturnal  seizures  in  the  second 
lady  were  probably  due  to  the  augmentation  of  blood-pressure  in 
the  arteries  occasioned  by  the  reciunbent  position  in  sleep.     This 


CHROMC  MYOCARDITIS  541 

at  length  overpowered  the  left  ventricle,  which  temporarily  became 
weaker  than  the  right,  and  acute  pulmonary  a'dema  supervened. 
In  some  of  these  cases  of  chronic  myocarditis  such  attacks  form 
the  principal  feature,  and  the  cases  are  particularly  grave  on  this 
account. 

Cases  of  Secondary  Valvular  Insufficiency. — Lastly,  one  occa- 
sionally meets  with  cases  of  myocardial  degeneration  which  mas- 
querade in  the  guise  of  a  mitral  or  aortic  regurgitation.  I  do  not 
refer  to  atheromatous  valvular  disease,  but  to  cases  in  which  the 
valvular  incompetence  is  relative  or  muscular.  Arthur  R.  Ed- 
wards has  reported  a  case  of  relative  aortic  insufficiency  from  ex- 
tensive myocardial  degeneration,  and  I  have  myself  observed  three 
cases  in  which  the  necropsy  revealed  the  same  condition.  In  all 
of  them  the  clinical  history  was  that  of  aortic  regurgitation. 

Mitral  incompetence  is  common  and  may  be  relative,  but  more 
often  is  muscular  from  degeneration  of  the  papillaries  or  slight 
ventricular  dilatation.  I  do  not  now  refer  to  Balfour's  Curable 
Mitral  Regurgitation,  which  is  seen  in  chlorosis  and  anaemia,  or 
to  that  form  seen  in  young  athletes  as  an  effect  of  acute  strain. 
These  all  yield  to  appropriate  treatment.  I  am  now  speaking  of 
left-ventricle  dilatation  and  secondary  mitral  insufficiency  seen  in 
cases  of  chronic  myocarditis.  I  have  under  observation  a  man  of 
sixty-five,  a  veteran  of  the  late  civil  war,  whose  mitral  valve  leaks 
in  consequence  of  great  dilatation  of  the  ventricle.  There  is  no 
history  of  inflammatory  rheumatism  or  any  other  disease  to  occa- 
sion endocarditis,  but  there  is  history  of  severe  physical  effort 
(climbing  a  mountain)  ten  years  ago.  Previous  to  that  strain  he 
had  no  cardiac  symptoms,  but  since  then  his  mitral  murmur  and 
dilatation  of  the  ventricle  have  been  present.  At  times  the  mur- 
mur wholly  replaces  the  first  sound,  but  as  the  ventricle  retracts 
under  treatment  by  baths  and  resistance  exercises,  the  first  sound 
becomes  audible  and  cardiac  impulse  palpable.  I  think  few  would 
venture  to  assert  that  in  this  case  the  myocardium  is  healthy. 

I  have  notes  of  the  case  of  another  gentleman  of  forty  who 
presented  the  signs  of  a  typical  mitral  regurgitation,  and  who  for 
four  years  struggled  to  preserve  his  compensation.  He  gave  a  his- 
tory of  mild  inflammatory  rheumatism,  of  gonorrhoea,  and  of  a 
thrombophlebitis  of  the  right  femoral  vein,  and  therefore  his 
valvular  incompetence  was  quite  naturally  supposed  to  be  of  endo- 


542  DISEASES  OF  THE   HEART 

carditic  origin,  a  conclusion  that  was  sti-engthened  by  the  occur- 
rence of  two  attacks  of  subacute  articular  rheumatism  during  the 
time  he  was  under  observation.  He  at  last  died,  after  having  been 
confined  to  his  bed  for  only  a  week,  with  symptoms  of  cardiac 
exhaustion.  There  was  no  o?dema,  very  insignifi.cant  venous  sta- 
sis, and  at  first  a  profound  sense  of  weakness  rather  than  of  short- 
ness of  breath.  Towards  the  close  of  his  illness,  however,  dyspna^a 
asserted  itself,  becoming  rather  spasmodic.  His  temperature 
grew  subnormal,  the  pulse  feebler  and  slightly  more  rapid,  and  he 
died  apparently  of  simple  cardiac  asthenia. 

The  necropsy  made  by  Dr.  W.  A.  Evans  disclosed  a  perfectly 
healthy  mitral  valve,  and  on  the  tricuspid,  chijnges  too  insignifi- 
cant to  have  aifected  their  function.  The  myocardium  was  in- 
tensely fatty,  particularly  of  the  right  ventricle ;  the  cavities  were 
all  more  or  less  dilated.  The  coronary  arteries  were  healthy,  but 
the  aorta  was  congenitally  small  throughout.  This  man  had  been 
an  athlete  in  college,  and  subsequent  to  his  death  I  learned  that 
before  his  symptoms  of  cardiac  inadequacy  began  he  had  over- 
strained his  heart  by  a  long,  hard  bicycle  ride.  Owing  to  the 
apparent  integrity  of  the  coronary  arteries  in  this  case,  I  believe 
there  can  be  only  two  explanation^;  of  his  myocardial  decay.  It 
was  either  an  expression  of  chronic  myocarditis  in  the  strict  sense 
of  toxic  origin,  or  of  a  disproportion  between  the  w^ork  required  of 
it  and  its  nutrition,  this  latter  being  restricted  by  reason  of  the 
congenital  smallness  of  the  aorta,  which  also  had  served  to  put 
undue  strain  upon  the  myocardium. 

Finally,  in  concluding  what  I  have  to  say  upon  the  symptoma- 
tology of  myocardial  inadequacy,  I  desire  to  add  a  few  words 
concerning  two  symptoms  which  are  generally  thought  indicative 
of  fatty  degeneration  of  the  heart.  These  are  yawning  and  sigh- 
ing. I  have  never,  however,  been  able  to  satisfy  myself  of  the 
import  of  these  two  symptoms.  Indeed,  I  not  only  have  seen 
many  cases  of  myocardial  inadeqmicy  in  which  they  were  absent, 
but  I  have,  on  the  other  hand,  observed  them  in  patients  who  pre- 
sented no  suspicion  of  myocardial  disease,  as  in  young  neurotic 
or  ana?mic  w^omen.  I  should  certainly  attach  no  value  to  yawning 
and  sighing  in  the  absence  of  other  less  doubtful  symptoms,  and 
in  suspected  cases  of  cardiac  degeneratioTi  I  should  esteem  them  of 
very  minor  importance. 


CHRONit  MYOCARDITIS 


543 


Physical  Signs. — Inspection. — In  most  cases  inspection  is 
negative.  If  the  eye  detects  signs  of  stasis,  there  is  nothing  in 
this  fact  to  indicate  the  underlying  condition.  The  general  ap- 
pearance of  the  individual  may  show  to  the  experienced  physi- 
cian signs  of  premature  or  senile  decay.  When  hypertrophy  of 
the  left  ventricle  is  present,  this  may  be  shown  by  the  displaced 
apex-beat.  But  in  the  class  of  cases  in  which  it  is  the  most  diffi- 
cult to  arrive  at  a  definite  conclusion — that  is,  middle-aged  and 
well-preserved  men  with  capacious  chests,  the  cardiac  impulse  is 
not  visible  becaiise  of  the  chest-capacity  and  lung-volume.  Conse- 
quently, it  may  be  said  that  the  chief  value  of  inspection  lies  in 
the  fact  of  its  negativeness,  for  other  disorders  of  the  heart  than 
myocardial  degeneration  are  very  apt  to  furnish  some  visible  indi- 
cation of  their  nature. 

Palpation. — This  is  of  value  in  the  determination  of  oedema 
and  of  hepatic  engorgement  even  more  than  in  the  examination 
of  the  heart.  Yet  by  careful 
palpation  of  the  prascordium 
one  is  often  able  to  locate  an 
apex-beat  which  is  too  feeble 
to  be  visible.  It  may  enable 
one  also  to  perceive  that  the 
cardiac  impulse  has  the  dif- 
fused jogging  character  of  dil- 
atation with  hypertrophy^,  or 
the  feeble,  slapping  shock  of 
dilatation.  Palpation  is  of 
special  value  in  disclosing  the 
state  of  the  arterial  coats.  If 
these  feel  thick  and  resisting, 
or  tortuous  and  uneven,  like  a 
string  of  beads,  they  furnish 
presumptive  evidence  that  the 
heart-muscle  is  not  sound.  In 
searching  for  signs  of  cardiac  incompetence  one  should  always 
endeavour  to  palpate  the  liver.  If  the  lower  border  of  this 
organ  can  be  felt  below  the  costal  arch,  and  particularly  if  it  is 
smooth,  rounded,  firm,  and  perhaps  tender,  there  is  hepatic  con- 
gestion, probably  secondary  to  more  or  less  cardiac  inadequacy. 


Fig.  103. — Showing  Shape  of  Kei.ative  Dul- 
NESs  IN  Hypekteophy.  Quadrilateral 
with  rounded  corners. 


544 


DISEASES   OF   THE   HEART 


Percussion. — This  means  of  investigation  should  never  be  neg- 
lected, for  verv  much  depends  upon  the  size  of  the  heart.  Abso- 
lute dulness  may  or  may  not  be  increased,  but  as  the  organ  is 
enlarged  in  most  cases  of  myocardial  degeneration,  careful  percus- 
sion usually  elicits  an  augmentation  in  the  area  of  cardiac  dulness. 
If  this  is  found  increased  to  the  left  and  upward,  it  indicates  left- 
ventricle  hypertrophy;  if  to  the  right  and  downward,  enlarge- 
ment of  the  right  ventricle.  In  general  cardiac  hypertrophy  the 
area  of  deep-seated  dulness  is  of  a  quadrilateral  outline  with 
rounded  corners  (see  Fig.  103). 

In  estimating  the  size  of  the  heart  it  is  customary  to  take  the 
left  verticle  nipple-line  as  the  normal  boundary  of  deep-seated 
dulness  at  the  left.  But  Fraentzel  dwells  particularly  on  the  lia- 
bility to  error  existing  in  the  custom  of  considering  the  left  nipple 
as  the  normal  boundary  of  relative  dulness  on  that  side.  If  the 
dulness  is  not  found  to  pass  beyond  this  mark  it  is  taken  for 
granted  that  the  size  of  the  heart  is  nornuil.     It  should  be  remem- 


Age. 

Weight. 

Height. 

Circumfer- 
ence of 
chest. 

Distance  from 

sternum  to  left 

nipple. 

K.  A 

29 
24 
25 
30 
28 
29 
42 
24 
24 
33 
23 
33 
28 
23 
23 
31 
If 

23 
21 
32 
29 
30 
30 
25 
25 
27 
24 
22 
43 

155 
135 
130 
150 
145 
157 
191 
149 
185 
170 
160 
125 
161 
195 
158 
145 
155 
140 
130 
165 

im 

135 
162 
189 
204 
150 
130 
145 
189 

Feet.       iDches. 

5        7 
5        7 
5        7 
5        9 
5         6 

5  9 

6  1 
5         6 
5         7 
5        8 
5       10 
5        4 
5        9 
5       10 

5               7:t 

5        9" 

5       n 

5       10' 
5         74 
(i         1 
5       10^ 
5        4 

5  H 

6  0 
6        0 
5        74 
5        6" 

5  8i 

6  0" 

Inches. 

33 

34 

34 

34 

34 

354 

40t 

36 

36 

36 

34 

30 

35 

40 

35 

34 

37 

334 

33 

35 

35i 

33 

38 

39 

39i 

38 

33 

35 

39 

Inches. 

H 

T.  B     

3 

C.  B 

E.B 

w.o 

S.  D 

3* 
3f 
H 
3i 

H.  De  V 

R.  E 

3f 
3i 

H 

3i 
21 

E.  E 

S.  E 

F.  G 

G.G 

C.  H 

H..I   

3i 
4 

P.  J 

G.  L 

L ... 

F.  M 

J.  M 

H.  M 

3 
3 

2* 
3* 

H.  S     

3i 
3 

J.  s 

J  S 

3i 
3i 

W.  V 

.F.  W 

.1.  \V 

4i 
3i 

J.  W 

3 

C 

3i 

C.  H 

3^ 

CHRONIC   MYOCARDITIS  545 

bered,  however,  that  the  distance  between  the  midsternal  and  left 
maniinary  lines  is  by  no  means  always,  the  case.  I  have  not  in- 
frequently found  the  left  nipple  situated  5  inches  from  the  mid- 
sternum.  Measurements  of  twenty-nine  of  my  students,  taken  for 
the  purpose  of  determining  variations  in  this  regard,  gave  the 
results  shown  in  the  table  on  the  opposite  page. 

These  figures  indicate  plainly  that  the  only  accurate  means  of 
determining  the  boundaries  of  the  heart  by  percussion  lies  in 
measuring  the  distance  to  which  the  area  of  deep-seated  dulness 
extends  to  the  left  of  the  median  line.  The  size  of  the  normal 
heart,  as  shown  by  percussion,  has  already  been  stated  in  the  in- 
troductory chapter. 

One  often  obtains  valuable  information  by  the  sense  of  in- 
creased resistance  on  firm  percussion,  and  hence  the  value  of 
Ebstein's  palpatory  percussion.  I  am  in  the  habit  of  verifying 
the  results  of  percussion  in  the  ordinary  way,  by  recourse  to  aus- 
cultatory percussion,  and  am  frequently  surprised  and  gratified  to 
see  how  closely  they  correspond. 

Auscultation. — Here,  too,  much  depends  upon  the  thickness 
or  thinness  of  the  chest-wall.  If  hypertrophy  exists  the  first  sound 
at  the  apex  is  prolonged  and  of  low  pitch,  while  the  second  is  usu- 
ally clear  and  ringing.  In  some  cases  the  systolic  sound  is  muf- 
fled and  indistinct.  At  the  base  of  the  heart  the  aortic  second 
is  sharply  accentuated,  ringing,  or  it  may  be  so  intense  as  to  be 
actually  banging.  There  is  also  intensification  of  the  pulmonic 
second  sound  when  the  left  ventricle  begins  to  fail,  and  at  the 
base  of  the  heart  one  sometimes  detects  reduplication  of  the  sec- 
ond sound.  If  the  first  in  the  region  of  the  apex  is  short  and 
sharp,  resembling  the  normal  second,  it  indicates  dilatation  rather 
than  hypertrophy. 

Occasionally  the  heart-sounds  take  on  the  canter-rhythm  de- 
scribed at  length  in  the  introductory  chapter.  This  character- 
istic rhythm  is  limited  to  one  or  the  other  ventricle,  and  there- 
fore to  the  neighbourhood  of  the  left  nipple.  It  is  especially 
likely  to  appear  in  left-ventricle  dilatation  consequent  upon  a 
granular  kidney,  but,  according  to  Fraentzel,  occurs,  although 
rarely,  in  enlargement  of  the  heart  from  other  causes.  This 
gallop  rhythm  must  be  kept  distinct  from  reduplication  of  the 

second  sound  heard  at  the  base,  and  from  that  apparent  or  simu- 
36 


546  DISEASES  OF  THE  HEART 

lated  doubling  of  the  second  sound  that  is  not  infrequently  dis- 
covered in  the  mitral  area  in  cases  of  stenosis  of  that  orifice. 

A  full,  tense,  not  accelerated  pulse,  a  dull  first  sound,  and  an 
accentuated  aortic  second,  form  a  combination  of  signs  highly  sug- 
gestive of  hyjDertrophy  of  the  heart,  even  though  its  area  of  rela- 
tive dulness  cannot  be  defined  with  certainty. 

There  is  no  pathognomonic  sign  of  degeneration  from  coro- 
nary sclerosis,  and  often  the  heart-sounds  appear  normal.  It  is 
highly  important,  however,  and  sometimes  yields  valuable  infor- 
mation, to  study  the  relative  pitch  and  intensity  of  the  several 
sounds.  If,  as  there  is  good  reason  to  believe,  one  of  the  elements 
entering  into  the  make-up  of  the  first  sound  is  a  muscular  ele- 
ment, imparting  to  the  sound  its  booming  quality,  and  caused  by 
contraction  of  the  ventricular  and  papillary  muscles,  then  impair- 
ment of  their  contractility  through  disease  should  theoretically 
diminish  the  intensity  of  the  first  heart-sound.  Experience  shows 
that  this  is  precisely  what  takes  place  in  some  instances.  Over 
the  weakened  left  ventricle  this  sound  at  the  apex  may  be  weaker 
than  that  over  the  right  ventricle,  having  a  distant  or  muffled 
character.  The  pitch  of  the  sound  may  be  raised  also  and  its  dura- 
tion somewhat  shortened.  The  second  sound  at  the  apex  is  often 
relatively  louder  than  the  systolic,  and  on  moving  the  stethoscope 
to  the  base  of  the  heart  this  intensification  of  the  second  sound  is 
found  due  to  accentuation  of  the  aortic  second,  which  may  even 
possess  a  ringing  character  from  sclerosis  of  the  aorta.  In  other 
cases  the  second  sound  at  the  right  of  the  sternum  is  feebler  than 
that  in  the  pulmonary  area. 

As  the  aortic  second  sound  should  be  the  louder  of  the  two 
in  persons  of  the  age  at  which  myocardial  degeneration  usu- 
ally develops,  relative  weakening  of  the  second  sound  in  the 
aortic  notch  points  to  diminished  vigour  in  ventricular  contrac- 
tions, and  honco  furnishes  indirect  evidence  in  favour  of  degen- 
eration. 

Murmurs  are  accidental  findings,  and  are  due  either  to  rela- 
tive incompetence  of  the  valves  or  to  atheromatous  roughening  of 
the  orifices.  In  either  event  they  may  afford  valuable  testimony  as 
to  the  state  of  the  heart-muscle.  A  murmur  may,  of  course,  in 
some  instances  be  the  result  of  a  rheumatic  valvular  defect,  as  will 
be  shown  by  the  history. 


CHRONIC  MYOCARDITIS  547 

Diagnosis. — From  the  foregoing,  it  is  evident  that  in  the 
diagnosis  of  degeneration  of  the  myocardium,  but  limited  in- 
formation is  derived  from  a  study  of  the  heart.  There  is  no 
form  of  cardiac  disease,  therefore,  in  the  diagnosis  of  which  so 
much  dej)ends  on  the  judgment  and  experience  of  the  physician. 
In  valvular  defects  there  are  murmurs  to  serve  as  guide-posts; 
in  hypertrophy  or  dilatation  there  is  obvious  alteration  of  size. 
In  the  affection  under  consideration  the  volume  of  the  organ  may 
or  may  not  be  changed,  and  therefore  great  dependence  must  be 
placed  on  age,  state  of  the  vessels,  history,  and  symptoms. 

Age  is  so  important  an  etiological  factor  that  the  development 
of  cardiac  insufficiency  in  an  individual  well  on  in  years  may  be 
set  down  to  degenerative  changes  with  tolerable  certainty.  It  is 
quite  otherwise  when  heart-weakness,  without  obvious  signs  of 
disease,  develops  in  a  person  about  the  middle  period  of  life.  In 
such  persons  careful  search  should  be  made  for  traces  of  prema- 
ture decay,  for  indications  of  renal  disease,  or  a  gouty  diathesis, 
etc.  There  is  an  old  saying  that  a  man  is  as  old  as  his  arteries, 
and  therefore  the  radials,  temporals,  and  other  peripheral  vessels 
should  be  carefully  palpated  for  evidences  of  thickening  or  for 
nodular  deposits  of  lime-salts. 

It  may  be  necessary  in  some  cases  to  make  an  ophthalmoscopic 
examination  of  the  retinal  artery  for  the  signs  of  sclerotic  change 
which  are  said  to  first  manifest  themselves  in  this  situation.  The 
physician  should  note  the  appearance  or  not  of  premature  whiten- 
ing of  the  hair,  and  examine  the  texture  of  the  skin.  I  have  more 
than  once  observed  that  persons  with  a  strong  suspicion  of  fatty 
degeneration  of  the  heart  have  a  skin  that  has  lost  its  elasticity 
and  feels  peculiarly  soft,  as  is  often  the  case  in  the  aged. 

The  examiner  should  scrutinize  the  fingers  and  ears  for  chalky 
deposits,  and  the  nails  for  those  longitudinal  ridges  said  to  be 
indicative  of  the  gouty  state.  In  this  way  valuable  hints  may 
often  be  obtained. 

The  wine  should  be  analyzed  carefully,  and  repeatedly  if  nec- 
essary, for  evidence  of  nephritis,  since  it  is  well  known  that  de- 
generation of  the  myocardium  is  a  frequent  accompaniment  of 
chronic  renal  disease,  particularly  the  interstitial  form. 

Minute  inquiry  into  the  patient's  history  may  elicit  facts  con- 
cerning family  tendencies,  personal  habits,  previous  diseases,  etc., 


548  DISEASES   OF   THE   HEART 

that  may  throw  light  upon  the  nature  of  the  present  malady.  It  is 
particularly  important  to  ascertain  whether  the  patient  has  suf- 
fered from  attacks  of  angina  pectoris  or  cardiac  asthma.  The 
significance  of  the  former  in  individuals  past  middle  age  is  very 
different  from  that  of  anginoid  seizures  in  adults  under  forty, 
especially  women. 

Even  in  spite  of  the  most  painstaking  investigation  and  atten- 
tion to  all  circumstances,  however  trivial,  a  positive  diagnosis  in 
this  class  of  cases  is  not  always  possible  without  awaiting  the 
results  of  therapeutic  management.  If  decay  of  the  heart-muscle 
is  present,  it  will  be  ultimately  shown  by  the  gradual  or  more 
rapid  development  of  symptoms  sufficiently  characteristic  to  settle 
the  diagnosis. 

Aneurysm  of  the  heart  is  only  possible  of  diagnosis  wdien  it 
is  of  sufficient  size  to  affect  the  outline  of  cardiac  dulness  in  a 
way  to  suggest  localized  bulging  of  the  heart-wall.  It  is  stated 
that  cardiac  aneurysm  may  be  suspected  when  there  is  a  striking 
disproportion  between  the  force  of  the  cardiac  impulse  at  or  near 
the  apex  and  the  smallness  and  feebleness  of  the  pulse.  Its  exist- 
ence can  probably  be  determined  by  fluorescopic  examination. 

In  most  cases  of-  cardiac  rupture  its  occurrence  can  only  be 
suspected  but  not  determined  before  the  death  of  the  patient.  It 
may  be  surmised  in  cases  running  the  extremely  acute  course  de- 
scribed in  Symptoms.  Physical  signs  pointing  to  fluid  disten- 
tion of  the  pericardium,  with  a  pale,  anxious  countenance,  a  small, 
feeble,  irregular,  it  may  be  intermittent  pulse,  and  other  symp- 
toms of  profound  shock,  furnish  strong  evidence  that  rupture  of 
the  heart-wall  has  taken  place.  If  life  is  sufficiently  prolonged 
a  correct  diagnosis  is  often  possible,  but  when  death  occurs  within 
a  few  minutes  the  physician  can  rarely  do  more  than  conjecture 
the  occurrence  of  rupture. 

The  diagnosis  of  chronic  myocarditis  is  largely  a  matter  of 
probabilities,  since  there  are  no  pathognomonic  signs  of  the  con- 
dition. Physical  examination  nuiy  disclose  certain  gross  changes, 
as  hypertrophy  or  dilatation,  or  a  combination  of  l)ot,li,  and  pathol- 
ogy teaches  that  such  hc^arts  arc  as  a  rule  more  or  less  degenerated, 
but  we  possess  no  means  of  determining  outside  the  dead-house  to 
what  extent  the  heart-muscle  is  diseased  or  the  precise  nature  of 
its  degeneration.    The  majority  of  elderly  individuals  who  consult 


CHRONIC  MYOCARDITIS  549 

lis  because  of  cardiac  symptoms  do  not  suffer  from  tlio  conse- 
quences of  rheumatic  endocarditis  as  do.  the  young.  Tliey  pre- 
sent evidence  of  cardiac  incompetence ;  of  this  we  can  he  certain, 
but  concerning  the  state  of  the  myocardium  we  must  take  much 
for  granted. 

Prognosis. — This  depends  upon  the  cause,  the  degree  of  the 
hypertrophy,  and  the  state  of  the  heart-muscle.  If  the  high  pulse- 
tension  is  due  to  luxus  consumption,  and  the  individual  is  young 
and  robust,  correction  of  his  habits  may  lessen  peripheral  resist- 
ance, and  may  retard,  if  not  wholly  prevent,  development  of  car- 
diac inadequacy.  In  cases  of  advanced  renal  or  vascular  disease 
there  are  two  dangers :  occurrence  of  apoplexy  and  the  breakdown 
of  the  heart  under  conditions  of  unwonted  strain.  If  the  cause, 
whatever  its  nature,  is  persistent  and  not  amenable  to  treatment, 
the  ultimate  prognosis  is  unfavourable,  because  there  will  at 
length  come  a  limit  to  the  hypertrophy  and  the  heart-wall  will 
give  way. 

So  long  as  the  myocardium  is  functionally  healthy — that  is, 
receives  sufficient  nourishment — the  hypertrophy  proves  a  pre- 
servative measure ;  but  when  incompetence  sets  in,  the  most  fa- 
vourable management  can  do  no  more  than  defer  the  evil  day. 
Palpitation,  and  particularly  intermittence  of  the  pulse,  are  unfa- 
vourable signs ;  they  may  be  the  first  evidence  that  the  heart  is 
yielding  to  the  unequal  struggle,  or  by  occasioning  incomplete 
emptying,  and  hence  distention  of  the  cardiac  chambers,  they 
may  hasten  the  coming  on  of  dilatation. 

In  forming  a  prognosis  in  any  given  case  one  must  take  into 
consideration  also  the  age  and  temperament  of  the  patient,  and 
the  state  of  his  general  nutrition.  The  younger  the  patient  and 
the  greater  his  self-control,  the  better  his  prospects  of  maintaining 
compensatory  hypertrophy  and  the  less  the  likelihood  of  injury 
from  excesses,  emotional  or  otherwise.  The  further  one  gets  be- 
yond middle  age  the  stronger  the  probability  of  the  cardiac  in- 
sufficiency being  due  to  myocardial  degeneration,  and  of  the 
obstacle  to  circulation  proving  too  much  for  the  weakened  heart- 
walls. 

When  serious  symptoms  at  length  set  in  there  is  small  pros- 
pect of  medical  skill  being  able  to  do  more  than  patch  up  the  crip- 
pled heart.     In  a  word,  the  prognosis  depends  upon  the  relation 


550  DISEASES  OF  THE   HEART 

existing  between  the  demands  made  npon  the  heart  and  its  ability 
to  respond.  It  is  therefore  abnost  entirely  a  qnestion  of  cardiac 
nutrition.  The  yonnger  the  individnal  the  less  the  likelihood  of 
serious  degenerative  changes,  but  after  middle  age  such  changes 
are  usually  present  and  compensatory  hypertrophy  is  rarely  re-es- 
tablished after  it  has  once  seriously  given  way.  One  should  make 
a  careful  study,  therefore,  of  the  condition  of  the  vascular  coats, 
as  they  furnish  presumable  indication  of  the  state  of  the  heart- 
muscle.  Nevertheless,  experience  teaches  that  the  latter  may  be 
extensively  diseased  while  the  arteries  appear  healthy.  The  de- 
tection of  the  gallop-rhythm  over  one  or  the  other  ventricle,  most 
often  the  left,  is  of  evil  import,  as  it  indicates  a  loss  of  muscu- 
lar tone  and  either  incipient  or  fully  developed  dilatation.  In 
the  cardiac  inadecpiacy  of  chronic  nephritis  this  symptom  may  be 
regarded  as  indicating  a  not  very  distant  termination  of  the  case. 

In  coronary  sclerosis  the  prognosis  is  most  grave.  We  pos- 
sess no  means  of  ascertaining  the  location  and  extent  of  degenera- 
tion, and  hence  cannot  say  whether  life  will  persist  a  single  hour. 
Indeed,  a  person  with  fatty  degeneration  of  the  heart-muscle  can 
never  be  sure  of  his  life  from  one  moment  to  another.  He  may 
live  for  years,  and  he  may  die  suddenly  when  apparently  in  the 
best  of  health. 

The  occurrence  of  angina  pectoris  makes  prognosis  doubly 
bad.  In  acute  and  subacute  cases  death  is  not  likely  to  be  long 
deferred,  and  except  in  the  most  acute  forms,  which  are  usually 
rapidly  fatal,  no  one  can  venture  to  predict  the  length  of  life. 
Chronic  forms  of  coronary  sclerosis  may  persist  for  many  years 
with  ever-recurring  attacks  of  angina.  As  a  rule  it  may  be  stated 
that  the  more  easily  and  frequently  pain  is  induced  the  graver  is 
the  prognosis. 

The  arrhyllimic  form  of  chronic  myocarditis  is  apt  to  run  a 
very  chronic  course,  wdiercas  those  showing  attacks  of  cardiac 
asthma  or  of  acute  pulmonary  oedema  are  in  danger  of  terminat- 
ing abruptly  in  such  an  attack.  The  development  of  Cheyne- 
Slokes  r(;spiration  is  in  most  instances  an  indication  tliat  the  end 
is  not  far  off  (see  article  on  this  type  of  breathing).  Syncopal 
attacks  are  likewise  of  evil  port(int,  owing  to  the  danger  of  sudden 
death  from  asystolism  at  such  times. 

The  cardiac  insufficiency  of  Uright's  disease  and  diabetes  is  of 


CHRONfC  MYOCARDITIS  551 

particularly  great  gravity,  since  the  abnormally  high  pulse-ten- 
sion, which  is  the  cause  of  the  cardiac  embarrassment,  cannot  be 
removed,  and  prevents  the  left  ventricle  from  regaining  its  lost 
power.  A  serious  breakdown  in  this  class  of  cases,  therefore,  may 
be  said  to  be  irreparable. 

Finally,  the  prognosis  is  also  determined  by  the  presence  or 
absence  of  sclerotic  changes  in  the  kidneys,  lungs,  and  liver,  since 
the  healthier  these  organs  the  less  the  strain  upon  the  diseased 
heart.  Chj'onic  gastritis,  with  its  flatulent  distention  of  the  hol- 
low viscera,  influences  prognosis  both  through  mechanical  pres- 
sure and  the  generation  of  injurious  toxines. 

Acute  bronchitis  or  other  illnesses,  in  particular  pneumonia 
and  influenza,  must  always  fill  the  medical  attendant  with  alarm, 
since  it  requires  but  little  to  throw  the  balance  one  way  or  the 
other  in  these  cases,  and  acute  infections  are  very  liable  to  prove 
the  immediate  cause  of  death  in  cases  of  chronic  myocarditis, 
which,  without  such  an  intercurrent  affection,  might  have  persisted 
for  years  longer.  Conditions  of  environment  also  affect  prognosis, 
an  individual  who  is  able  to  spend  his  winters  in  a  mild  climate 
and  avail  himself  of  all  other  means  of  warding  off  injurious  in- 
fluences being,  ceteris  'paribus,  likely  to  live  longer  than  he  who  is 
compelled  to  toil  on  for  his  daily  bread. 

In  conclusion  may  be  quoted  Huchard's  emphatic  statement 
concerning  cases  of  myocardial  disease :  "  Their  evolution  is 
latent,  their  beginnings  insidious,  their  course  paroxysmal,  their 
progress  interrupted,  their  visceral  complications  various,  and 
their  explosions  of  cardiac  insufficiency  are  sudden." 

Treatment. — This  must  be  considered  first  with  regard  to 
preservation  of  cardiac  competence,  and  second  with  reference  to 
the  stage  in  which  heart-power  is  either  showing  signs  of  failure 
or  has  actually  been  lost — pronounced  cardiac  insufficiency. 
Medical  aid  is  not  sought  so  long  as  the  myocardium  is  adequate, 
and  if  the  discovery  of  hypertrophy  is  made,  it  is  only  by  accident. 
When,  however,  such  discovery  is  made,  it  should  be  the  physi- 
cian's duty  to  call  the  j)atient's  attention  to  the  dangers  threaten- 
ing him  in  the  future,  and  to  show  him  how  his  habits  of  life  are 
likely  to  affect  his  heart. 

The  management  is  now  along  the  line  of  prevention ;  patients 
who  habitually  eat  or  drink  too  much  must  have  the  evils  of  glut- 


552  DISEASES  OF  THE  HEART 

tonj  explained  to  them,  and  be  put  upon  a  diet  that  will  not  over- 
tax kidneys,  vessels,  and  heart.  The  man  who  takes  little  or  no 
exercise,  and  is  too  rapidly  gaining  weight,  must  be  sent  to  the 
gymnasium  to  be  put  in  training,  or  must  be  made  to  walk  more 
and  ride  less. 

//  vessels  are  sound  and  heart  still  competent  there  is  noth- 
ing better  for  such  patients  than  moderate  bicycling,  tennis,  ball- 
playing,  etc.  If  such  sports  are  thought  too  vigorous,  there  is 
golf,  which  is  an  ideal  form  of  exercise,  since  it  trains  the  eyes 
and  muscles  without  subjecting  weak  organs  to  undue  strain. 
Those  with  corpulent,  flabby  abdomen  are  much  benefited  by  a 
course  of  massage  and  Swedish  movements.  .The  processes  of 
digestion  and  assimilation  are  improved,  and  constipation,  if 
present,  is  generally  corrected. 

Gouty  individuals  or  persons  suffering  from  defective  excre- 
tion usually  derive  benefit  from  a  semi-weekly  or  a  weekly  Turk- 
ish bath.  This  not  only  increases  elimination,  but  lessens  blood- 
pressure.  This  seems  especially  beneficial  to  persons  addicted  to 
the  abuse  of  alcohol  and  tobacco.  If  the  cause  of  the  hypertrophy 
is  not  preventable,  or  if  vascular  and  renal  changes  are  pro- 
nounced, then  patients  should  be  frankly  informed  of  their  con- 
dition, and  warned  against  undue  muscular  effort,  or  whatever 
may  serve  as  an  additional  and  unnecessary  strain  to  the  heart- 
muscle.  Arterial  and  kidney  disease  call  for  still  greater  strict- 
ness in  the  matter  of  diet. 

A  highly  nitrogenous  dietary  often  serves  to  intensify  the 
already  existing  high  arterial  tension,  while  a  vegetarian  diet,  or 
one  bordering  thereon,  lowers  blood-pressure. 

Digestive  disturbance  and  constipation  must,  if  possible,  be 
corrected,  since  they  not  only  increase  arterial  tension,  but  may 
produce  palpitation  and  intermittence,  which,  if  allowed  to  go  on, 
may  ultimately  impair  the  integrity  of  the  heart-muscle,  which 
in  this  stage  it  is  our  aim  to  preserve. 

Cardiac  tonics,  especially  digitalis,  are  not  needed  at  this 
time,  and  if  administered  are  likely  to  do  harm.  Our  attention 
is  to  be  addressed  not  to  the  heart  itself,  but  to  its  protection  from 
all  injurious  influences. 

Unless  induced  acutely  by  severe  heart-strain,  signs  of  inade- 
quacy begin  to  declare  •tliomselves  slowly  and  at  first  very  insidi- 


CHRONIC  Myocarditis  553 

onsly,  so  that  the  maiiagciiicnt  may  bo  said  to  pass  almost  im- 
perceptibly into  tlie  treatment  of  symptoms  directly  due  to: 

Commencing  Loss  of  Heart-power. — Among  the  earliest  signs 
of  this  second  stage  may  be  tachycardia  and  palpitation.  These 
do  not  indicate  excessive  hypertrophy,  for  snch  does  not  exist, 
bnt  are  tokens  that  the  organ  is  finding  its  work  too  heavy. 
Therefore  an  attempt  shonld  be  made  to  discover  and  remove 
possible  sources  of  irritation  and  increased  peripheral  resistance 
before  aconite  or  veratrum,  digitalis,  or  strophanthns  are  pre- 
scribed. The  former  are  powerful  cardiac  depressents  and  must 
be  used  carefully,  but  in  the  past  three  years  have  been  employed 
by  me  frequently.  The  precise  indications  for  their  use  cannot  be 
stated,  but  seem  to  be  a  dangerously  high  blood-pressure  with  con- 
sequent strain  of  the  heart-walls. 

A  too  rapid  or  violent  action  of  the  heart  in  this  stage  may  be 
due  to  digestive  disorders,  constipation,  or  faulty  elimination 
which  raise  blood-pressure  and  hence  subside  with  removal  of  the 
cause.  To  this  end  I  find  very  satisfactory  a  periodic  dose  of 
calomel,  or  blue  pill  followed  by  an  aperient  water. 

It  may  be  well  to  restrict  the  diet  by  cutting  down  the  red 
meats  and  limiting  the  total  amount  of  water  and  other  fluids 
which  is  taken  by  the  patient.  The  former  raise  pulse-tension 
by  reason  of  their  extractives,  while  the  latter  distend  the  stom- 
ach and  abdominal  vessels,  thus  increasing  the  strain  on  the  left 
ventricle. 

Should  blood-pressure  still  be  too  high,  it  may  be  reduced  by 
one  of  the  nitrites  or  by  an  iodide.  Three  to  five  grains  of  potas- 
sium iodide  may  be  given  in  essence  of  pepsin  after  meals  with- 
out disturbing  the  stomach,  or  nitroglycerin,  to -g-  of  a  grain,  may 
be  given  every  three  hours.  Erythrol  is  said  to  be  more  lasting 
in  its  effects  on  the  arterioles,  but  this  advantage  has  not  seemed 
to  me  sufficient  to  compensate  for  its  greatly  increased  cost. 

Should  such  treatment  fail  to  control  cardiac  action,  then  it  is 
well  to  resort  to  digitalis  or  allied  remedies.  They  may  be  given 
in  conjunction  with  iron,  arsenious  acid,  or  strychnine. 

Gentle  exercise  is  now  very  beneficial  by  its  action  on  the 
heart  and  vascular  system. 

It  causes  dilatation  of  the  intermuscular  arterioles,  promotes 
venous  flow,  and  thus  tends  to  restore  circulatory  equilibrium,  re- 


554  DISEASES  OP  THE   HEART 

moves  waste  products  from  the  tissues,  and  flushes  the  heart-muscle 
with  freshly  oxygenated  blood.  This  explains  why  patients  who 
feel  priecordial  ojipression  upon  starting  out  for  a  walk  often  ex- 
perience a  sense  of  relief  and  well-being  after  their  exercise  has 
"  warmed  them  up,"  as  they  say. 

Gentle  pedestrian  exercise  is  to  be  recommended,  therefore,  in 
this  stage  of  commencing  cardiac  incompetence,  but  under  certain 
restrictions.  Patients  must  be  cautioned  to  begin  their  walk  at  a 
slow  pace,  and  to  increase  their  speed  only  as  they  find  exercise 
and  breathing  grow  easier.  Walking  against  a  cold  or  strong 
wind  is  very  trying,  and  on  such  days  they  should  walk  with  and 
not  in  the  face  of  such  wind.  The  carrying  of,  heavy  parcels  is  to 
be  forbidden,  and  the  restraint  of  trunk  or  limbs  by  tight  clothing 
is  inadmissible. 

The  ascent  of  stairs  and  hills  is  fraught  with  danger  to  the 
failing  heart,  and  should  be  avoided.  Oertel's  plan  of  hill-climb- 
ing is  to  be  advised  only  for  patients  whose  hearts  still  retain  a 
fair  measure  of  their  integrity  and  whose  judgment  can  be  relied 
upon.  The  principle  underlying  this  mode  of  treatment  consists 
in  the  ascent  of  gentle  inclines  at  a  rate  of  speed  that  does  not 
cause  dyspnoea  or  palpitation.  Only  when  such  acclivity  can  be 
surmounted  with  ease  is  a  steeper  grade  to  be  allowed.  If  hill- 
climbing  is  done  so  as  not  to  occasion  respiratory  or  circulatory 
embarrassment,  the  heart-walls  are  gradually  strengthened  and  a 
tendency  to  dilatation  is  overcome.  This  form  of  exercise  requires 
excellent  judgment  on  the  part  of  the  patient  lest  he  overdo,  and 
on  the  part  of  the  physician  in  the  selection  of  suitable  cases. 

Another  kind  of  cardiac  exercise  not  open  to  the  same  objec- 
tion, and  suited  to  a  larger  number  of  cases  becauses  its  effects 
can  be  more  accurately  gauged,  arc  the  "  resistance  exercises," 
which  were  described  in  detail  in  the  chapter  devoted  to  Treat- 
ment of  Valvular  Disease.  If  golf  is  permitted  to  patients  in  this 
stage  of  deficient  cardiac  power  it  sliould  be  restricted  to  put- 
ting, or  at  most  to  the  playing  of  a  liiiiited  mnnber  of  holes. 
Whatever  tlie  form  of  outdoor  exercise  allowed,  the  following 
restrictions  should  be  imposed:  (1)  Patients  must  not  exer- 
cise immediately  after  eating,  the  length  of  time  devoted  to 
rest  being  determined  by  the  degree  of  cardiac  weakness.  In 
most  cases  patients  should  remain  ([uiet  for  at  least  an  hour,  and 


CHRONIC  •  MYOCARDITIS  555 

when  the  heart  is  feeble  Fracntzel  does  not  allow  exercise  before 
three  or  four  hours  after  a  meal.  (2)  Walking  or  other  exercise 
should  not  be  indulged  in  to  the  point  of  fatigue.  In  some  cases 
indeed  it  should  be  for  only  a  short  period,  several  times  repeated 
during  the  day.  (3)  In  cases  showing  decided  indications  of  a 
threatened  loss  of  adequacy,  rest  in  a  recumbent  posture  must  be 
insisted  on  at  the  close  of  exercise. 

As  our  aim  at  this  time  is  to  prevent  the  heart  from  becoming 
still  more  taxed  in  its  labours,  and  blood-pressure  is  increased  by 
hearty  feeding,  it  is  necessary  to  restrict  the  diet.  It  is  quantity 
even  more  than  quality  that  is  harmful,  and  hence  patients  should 
be  told  to  eat  lightly.  Too  much  liquid  raises  blood-pressure  in 
the  abdominal  vessels,  and  therefore  it  is  well  to  restrict  it  to  8 
or  at  most  10  ounces  with  each  meal.  Alcoholic  stimulants,  if 
permitted  at  all,  must  be  in  the  form  of  a  light,  dry  wine,  or  still 
better  of  a  modicum  of  whisky,  largely  diluted  with  water.  To- 
bacco is  to  be  allowed  in  great  moderation,  a  small  light  cigar  or 
a  single  pipeful  of  mild  tobacco  after  meals.  Huchard,  Fraent- 
zel,  Krehl,  and  others  are  very  strenuous  in  their  opposition  to 
strong  Havana  cigars  on  the  ground  that  they  augment  arterial 
tension,  and  state  that  many  middle-aged  men  with  weak  hearts 
find  out  for  themselves  that  they  are  obliged  to  substitute  mild 
domestic  cigars  for  the  heavy  Havana  ones  to  which  they  have 
been  accustomed. 

Excesses  of  all  kinds  are  injurious,  and  these  patients  are  to 
be  warned  against  the  harmful  effect  of  frequent  sexual  indul- 
gence. Indeed,  the  principle  that  must  govern  the  daily  life  of 
these  individuals  is  moderation  in  all  things.  If  patients  give  due 
heed  to  the  doctor's  admonitions  they  may  succeed  in  holding  their 
hearts  in  statu  quo  for  a  considerable  time.  Unfortunately,  how- 
ever, the  tendency  of  myocardial  decay  is  downward,  and  hence 
we  are  called  on,  soon  or  late,  to  institute  active  treatment  for  the 
relief  of  symptoms  which  mark  the  arrival  of  the  third  stage. 

Cardiac  Incompetence  Pronounced. — Venous  and  visceral 
congestion  now  begins  to  manifest  itself,  and  calls  for  the  more 
vigorous  and  frequent  use  of  cathartic  remedies.  It  is  also  gen- 
erally necessary  to  resort  to  cardiac  tonics,  and  of  these  digitalis 
heads  the  list,  although  strophanthus,  spartein,  convallaria,  adonis 
vernalis,  and  caffeine  are  all  useful.    Whenever  digitalis  is  admin- 


556  DISEASES  OF   THE   HEART 

istered  to  a  patient  who  exhibits  higli  pulse-tension,  particnhirly  if 
this  depends  on  arterial  thickening,  it  should  always  be  given  in 
conjunction  with  an  iodide  salt  or  nitroglycerin  to  counteract  its 
effect  on  the  arterioles.  So  long  as  cardiac  weakness  is  not  ex- 
treme the  dose  of  digitalis  may  be  small,  10  drops  of  a  fat-free 
tincture  thrice  daily,  or  15  drops  every  twelve  hours.  Given  in 
this  way  it  may  be  continued  for  weeks  or  even  months  without 
losing  its  effect  or  exhibiting  its  cumulative  action.  In  more  than 
one  instance  of  myocardial  inadequacy  with  stiff  arteries  I  have 
seen  striking  results  follow  the  prolonged  use  of  strophanthus. 
It  is  sometimes  well  to  combine  these  two  remedies,  a  few  drops  of 
each  being  taken  at  a  dose.  Spartein  sulphate  is  highly  recom- 
mended by  the  French  when  the  pulse  is  irregular,  but  although 
I  have  tried  it  repeatedly  I  have  never  been  able  to  satisfy  myself 
of  its  beneficial  effect  or  advantage  over  digitalis. 

Strychnine  is  so  indispensable  a  heart-tonic  that  I  believe  it 
should  be  taken  by  this  class  of  cardiopaths  as  regularly  as  is  their 
food.  A  fortieth  or  even  a  thirtieth  of  a  grain  three  times  a 
day  is  not  at  all  too  much  for  the  average  patient. 

The  one  form  of  treatment  from  which  I  have  seen  patients 
with  myocardial  insufficiency  derive  most  benefit  are  the  natural 
or  artificial  Nauheim  baths  (see  page  466).  They  should  be  com- 
bined with  resistance  exercises.  In  my  opinion  this  form  of  treat- 
ment is  particularly  adapted  to  this  class  of  cardiopaths,  and  I 
have  rarely  seen  a  case  of  dilated  hypertrophy  which  has  not  been 
improved  by  its  judicious  employment.  I  recall  a  typical  example 
of  this  form  of  heart-disease  in  a  medical  man  of  forty-four,  who 
began  to  manifest  symptoms  of  threatening  dilatation.  His  area 
of  absolute  cardiac  dulness  was  greatly  increased,  particularly  to 
the  left,  and  anything  more  than  moderate  exercise  occasioned  a 
very  considerable  degree  of  discomfort.  Six  weeks  of  baths  com- 
pletely restored  the  heart's  power,  and  although  five  years  have 
now  elapsed,  the  doctor  is  still  able  to  attend  to  the  duties  of  a 
large  and  exacting  practice.  His  professional  calls  have  required 
him  to  daily  clind)  many  flights  of  stairs,  and  although  unwonted 
exertion  still  calls  forth  some  degree  of  l)rcathlessness,  he  has,  by 
keeping  down  his  pulse-tension  through  a  somewhat  restricted  diet 
and  an  occasional  -purgative,  never  again  displayed  the  same 
threatening  symptoms.     The  last  time  I  heard  from  him  he  had 


CHRONIC  MYOCARDITIS  557 

taken  to  a  bicycle,  and  by  careful  riding  succeeded  in  still  further 
strengthening  his  heart.  At  the  close  of  hi's  course  of  baths  abso- 
lute dulness  had  returned  to  normal,  and  the  relative  become 
manifestly  reduced.  He  weighed  over  200  pounds,  and  of  course 
still  has  a  considerable  degree  of  cardiac  hypertrophy.  In  the 
summer  of  1899  I  treated  by  means  of  baths  and  resistance  exer- 
cises two  middle-aged  gentlemen,  each  with  enormous  hyper- 
trophy. The  symptom  chiefly  complained  of  by  one  was  great 
pra3Cordial  oppression,  amounting  almost  to  what  Gairdner  would 
call  "  angina  sine  dolore,^^  whenever  walking  was  attempted  about 
an  hour  after  meals.  His  pulse  was  slow  and  tense,  and  his  heart 
enormously  enlarged.  At  the  end  of  treatment  the  heart  was  not 
much  reduced  in  size,  but  the  sounds  were  manifestly  stronger, 
and  the  pulse  had  become  fuller,  stronger,  and  slightly  more  rapid. 
He  then  passed  a  month  at  his  summer  cottage,  where  he  daily 
indulged  in  light  carpentering,  and  was  able  to  ascend  the  sandy 
hill  on  which  his  home  stood  without  experiencing  the  former 
discomfort.  A  very  restricted  diet  and  the  daily  use  of  small 
doses  of  the  tincture  of  strophanthus  and  iodide  of  sodium  have 
been  rewarded  by  continued  improvement.  The  second  patient 
also  derived  much  benefit  from  the  baths  and  exercises,  although, 
as  in  the  preceding  case,  the  area  of  deep-seated  cardiac  dulness 
did  not  become  permanently  diminished.  I  was  frequently  able 
to  determine  a  reduction  in  the  size  of  the  heart  following  a  bath, 
and  he  always  experienced  a  sense  of  well-being  and  lightness  in 
the  chest.  In  this  case  there  was  a  very  obstinate  indigestion,  and 
the  urine  always  contained  an  excess  of  solids,  although  it  never 
showed  albumin  or  casts.  His  pulse  was  for  the  most  part  irregu- 
lar and  intermittent,  seeming  to  be  governed  in  this  respect  by  the 
intestinal  indigestion,  for  every  time  his  digestive  disturbance 
became  aggravated  his  pulse  grew  more  irregular.  He  was  subse- 
quently induced  to  take  a  course  of  massage  and  Swedish  gymnas- 
tics, with  the  result  that  not  only  did  his  corpulent  abdomen  be- 
come greatly  reduced  in  size,  but  his  digestion  improved,  his  pulse 
became  regular  for  days  together,  and  he  said  he  felt  as  well  as  he 
ever  did  in  his  life.  The  heart,  however,  still  showed  great  en- 
largement. 

In  both  these  cases  a  change  of  habit  as  to  food  and  exer- 
cise lowered  blood-pressure,  treatment  of  the  heart  restored  its 


558  DISEASES  OF   THE  REART 

competence,  and  threatening  dilatation  was  averted.  I  should  add 
that  all  these  three  patients  continued  their  professional  and  busi- 
ness duties  while  undergoing  treatment. 

In  most  cases  that  have  reached  this  stage  restoration  of  heart- 
power  is  out  of  the  question.  The  problem  confronting  the  physi- 
cian is  how  to  relieve  symptoms  and  postpone  the  final  catas- 
trophe. In  such,  exercise  is  likely  to  do  harm  instead  of  good, 
and  yet  my  experience  has  convinced  me  that  harm  is  also  likely 
to  result  from  a  too  rigid  enforcement  of  rest.  If  the  breakdown 
is  complete,  the  sufferer  may  be  forced  to  remain  in  bed  or  his 
easy  chair.  If  things  have  not  reached  this  pass,  I  believe  it  is 
better  to  allow  the  invalid  to  move  quietly  about  his  room  that 
venous  circulation  may  be  aided  by  muscular  contraction  and  the 
deepened  respiration  consequent  upon  this  exercise.  In  some  in- 
stances venous  circulation  may  be  assisted  by  gentle  massage,  and 
carefully  conducted  resistance  exercises  may,  by  dilating  the 
arterioles,  and  thus  flushing  the  muscles,  help  to  unload  the  over- 
distended  heart. 

Romberg  and  Fraentzef  are  both  emphatic  concerning  the  in- 
jury of  too  strictly  enforced  rest  in  chronic  myocarditis,  and  expe- 
rience has  convinced  me  of  the  soundness  of  their  advice.  In  the 
earlier  years  of  my  practice  I  used  to  consider  prolonged  rest  indi- 
cated in  all  cases  of  cardiac  incompetence  from  whatever  cause, 
but  I  ultimately  found  that  elderly  individuals,  who  were  not 
suffering  from  valvular  disease,  showed  an  acceleration  of  their 
downward  course  when  they  were  denied  all  exercise  and  kept  rig- 
orously in  bed. 

The  aggravation  of  symptoms  thus  resulting  is  attributed  by 
Romberg  to  the  enervating  effects  of  inaction,  the  same  as  is  ob- 
served in  the  case  of  the  voluntary  muscles  from  disuse.  The 
same  thing  is  observed  in  previously  healthy  persons  who  are 
obliged  to  remain  in  bed  a  long  time,  from  one  cause  or  another; 
when  again  permitted  to  get  up  they  not  only  find  their  legs  weak, 
but  the  first  attempt  at  walking  produces  slight  shortness  of  breath 
and  acceleration  of  the  pulse.  This  explanation  is  in  accordance 
with  that  given  by  Fraentzel,  and  is  doubtless  correct  so  far  as  it 
goes.  In  the  case  of  a  degenerative  heart,  there  is  another  reason 
whicli  I  thiiik  holds  good.  When  a  patient  remains  quiet  in  a 
recumbent  position  the  venous  circulation  is  deprived  of  two  fac- 


CHRONIC  'MYOCARDITIS  559 

tors  of  great  importance  in  its  maintenance.  These  are  muscular 
effort  and  deepened  respiration.  Muscular  contraction  aided  by 
the  venous  valves  exerts  a  pumping  action  on  the  venous  current, 
and  also  the  flow  within  the  absorbents.  Abolish  the  use  of  the 
muscles  and  you  remove  one  of  the  well-known  causes  of  venous 
circulation.  Furthermore,  with  rest  in  bed  the  patient  breathes 
more  slowly  and  superficially,  and  hence  blood  is  less  rapidly  aspi- 
rated out  of  the  great  veins  into  the  right  heart,  and  a  second 
important  factor  in  maintaining  venous  flow  is  diminished. 

The  work  of  maintaining  the  circulation  now  devolves  upon 
the  heart  even  more  than  under  normal  conditions.  It  must  con- 
tract more  powerfully  that  its  driving  force  may  be  felt  through- 
out the  entire  circle  propelling  the  blood  onward  in  the  veins.  Tn 
those  cases  in  which  breathlessness  on  effort  is  a  pronounced  fea- 
ture absolute  rest  for  a  time  may  be  beneficial,  hut  it  will  not  do 
to  let  these  ijcitients  remain  quiet  for  too  long  a  iieriod. 

The  heart-muscle  is  weak,  and  cannot  be  left  for  too  long  a 
time  to  cope  unaided  with  the  labour  of  maintaining  adequate 
blood-flow.  Instead,  therefore,  of  complete  rest,  it  is  better  that 
the  physical  repose  be  interrupted  by  short  periods  of  gentle  exer- 
cise. This  last,  however,  is  to  be  strictly  controlled.  The  patient 
must  only  be  allowed  to  walk  about  his  room,  or  at  the  most  into 
the  adjoining  room.  Under  no  circumstances  is  he  to  be  allowed 
to  climb  stairs  nor  to  walk  about  soon  after  a  meal.  He  must  be 
impressed  with  the  danger  of  jumping  up  suddenly  and  of  hurry- 
ing across  the  room.  If  very  weak,  and  dyspnoea  is  considerable, 
he  had  better  lean  upon  the  arm  of  an  attendant  while  taking  his 
•  exercises. 

The  patient  should  also  not  be  allowed  to  dress  himself  un- 
aided, and  he  must  be  instructed  not  to  strain  at  micturition  or 
defecation,  since,  according  to  Sommerbrodt,  straining  during 
such  acts  raises  blood-pressure  reflexly,  and  has  more  than  once 
caused  sudden  diastolic  arrest  of  the  left  ventricle. 

If  massage  is  employed  it  must  not  be  applied  to  the  abdomen, 
unless  very  cautiously,  since  it  raises  blood-pressure.  Also,  if  re- 
sistance exercises  form  a  part  of  the  management  at  this  time, 
those  are  not  permissible  which  constrict  the  abdomen  or  necessi- 
tate the  elevation  of  the  arms  to  a  level  above  the  patient's  head, 
as  they  are  likely  to  occasion  dyspnoea  and  do  harm. 


560  DISEASES   OF   THE   HEART 

In  the  matter  of  food,  it  is  well  to  reniomber  that  these  patients 
require  a  relatively  small  amount  of  nourishment  on  account  of 
the  enforced  inactivity  of  their  lives.  They  should  consume  a  lim- 
ited quantity  of  liuids,  since  it  is  an  easy  matter  to  ingest  more 
than  can  be  excreted  by  the  kidneys  because  of  congestion,  and 
only  such  an  amount  is  to  be  allowed  as  is  found  by  actual  trial 
to  promote  the  renal  function.  Special  care  is  to  be  had  in  order- 
ing such  foods  as  do  not  induce  flatulent  distention  of  the  stomach 
and  bowels,  and  when  this  occurs  it  must  be  relieved  by  carmina- 
tives and  medicines  that  assist  feeble  digestion. 

Of  equal  importance  with  the  prevention  of  fermentative  indi- 
gestion is  the  correction  of  constipation.  This  is  injurious  not 
only  because  it  necessitates  straining  at  stool,  but  also  on  account 
of  its  raising  arterial  blood-pressure,  and  thereby  increasing  dys- 
pnoea, and  the  liability  to  attacks  of  angina  pectoris  and  cardiac 
asthma.  The  patient  should  therefore  take  a  laxative  pill  at  bed- 
time, containing  some  of  the  well-known  combinations  of  aloes, 
cascara,  podophyllin,  rhubarb,  and  colocynth,  or  a  morning 
draught  of  some  aj^erient  water.  It  will  not  do  to  purge  these 
patients  repeatedly  and  violently,  since  there  is  danger  of  aug- 
menting the  already  existing  debility,  and  yet  a  considerable 
degree  of  hepatic  engorgement  may  render  necessary  an  occasional 
sharp  purge. 

Having  in  this  way  endeavoured  to  remove  or  lessen  the  vari- 
ous conditions  which  may  embarrass  heart-action,  the  medical 
adviser  should  next  turn  his  attention  to  those  therapeutic  meas- 
ures which  usually  afford  a  prf)spect  of  strengthening  the  heart- 
muscle.  Digitalis  is  the  agent  usually  employed  in  this  as  well  as 
other  forms  of  cardiac  debility.  It  should  be  prescribed,  however, 
with  care  and  judgment.  If  the  heart-muscle  is  greatly  damaged, 
it  is  not  likely  to  respond  to  the  remedy,  which  will  then  exert 
itself  chiefly  on  the  arterioles.  Through  contraction  of  the  latter 
blood-pressure  is  raised,  so  that  instead  of  strengthening  the  heart 
digitalis  may  actually  increase  its  labour.  If  given  in  such  a  case, 
the  remedy  should  be  prescribed  in  moderate  doses,  5  or  10  drojis 
of  the  tincture,  twice  or  thrice  daily,  and  its  constricting  effects  on 
the  vessels  should  be  counteracted  by  nitroglycerin. 

In  coronary  sclerosis  the  nature  of  the  degenerative  changes 
that  take  place  in  the  heart  jirecludes  the  possibility  of  doing  any- 


CHRONie  MYOCARDITIS  561 

tiling  more  than  to  relieve  symptoms.  In  the  most  acute  manifes- 
tations of  the  disease,  the  physician,  ^vllo.  has  been  hastily  sum- 
moned, is  usually  able  to  do  no  more  than  attest  the  fact  of  death. 
In  the  somewhat  less  acutely  fatal  cases  with  manifestations  of 
profound  shock  stimulation  is  urgently  indicated.  Time  should 
not  be  lost  by  sending  for  some  favourite  stimulant,  but  use  should 
be  made  of  whatever  is  at  hand.  A  tablet  of  nitroglycerin,  with 
which  every  physician  is  usually  provided,  may  be  placed  upon 
the  tongue ;  and  while  an  attendant  follows  this  with  ^  an  ounce 
of  whisky  or  brandy,  the  physician  should  inject  under  the  skin 
-J  of  a  grain  of  morphine.  Twenty  drops  of  spirits  of  cam- 
phor, or  ^  a  drachm  of  aromatic  spirits  of  ammonia,  j)i"op6rly 
diluted,  is  also  an  efficient  stimulant,  and  may  be  repeated  at  inter- 
vals of  twenty  minutes.  Meanwhile,  members  of  the  family 
should  fill  bottles  with  hot  water  and  place  them  about  the  body 
and  limbs  of  the  patient,  who  is  then  to  be  wrapped  in  blankets. 
A  hot  bag  or  bottle  should  also  be  j^laced  at  the  pra^cordium. 

By  these  and  other  means  every  attempt  is  to  be  made  to  restore 
the  failing  circulation.  In  some  cases,  unfortunately,  all  efforts 
are  unavailing,  but  should  the  patient  rally  somewhat,  stimulation 
is  to  be  continued  in  such  doses  and  at  such  intervals  as  will  main- 
tain the  heart's  action.  If  after  the  lapse  of  a  few  hours  it  be 
thought  best  to  administer  food  to  the  patient,  this  should  be 
liquid  and  hot,  as  a  cupful  of  soup  or  hot  milk,  to  which  the  am- 
monia, whisky,  or  brandy  may  be  added.  It  may  now  be  well  to 
order  strychnine  hypodermically,  in  doses  of  :o^  or  ^V  of  a  grain 
every  two  or  three  hours ;  but  digitalis,  strophanthus,  and  the 
like  are  contra-indicated  or  are  to  be  given  cautiously. 

If  the  initial  symptom  is  an  attack  of  angina  pectoris,  nitro- 
glycerin, 1  minim,  and  ^  of  a  grain  of  morphine  under  the  skin, 
will  probably  afford  relief,  and  may  be  followed  by  hot  whisky, 
and  hot  applications  to  the  extremities  and  pra?cordium,  the  subse- 
quent use  of  stimulants  being  left  to  the  judgment  of  the  attend- 
ing physician. 

In  subacute  cases,  which  run  their  course  in  a  few  weeks,  or  at 
the  most  in  a  few  months,  the  serious  changes  which  the  heart- 
muscle  has  undergone  place  the  restoration  of  compensation  out 
of  the  question.  Both  the  physician  and  patient  must  concern 
themselves  with  such  measures  as  tend  to  make  the  downward 
37 


562  DISEASES  OP  THE   HEART 

career  as  slow  as  possible.  What  strength  the  heart  still  retains 
must  be  carefully  preserved,  and  all  unnecessary  demands  upon 
it  studiously  avoided. 

The  management  of  chronic  cases  of  coronary  sclerosis  is  also 
largely  preventive  and  symptomatic,  but  there  is  often  enough  re- 
serve power  left  in  the  organ  for  considerable  improvement  fol- 
lowing measures  calculated  to  roinstatc  the  heart-muscle  to  a  lim- 
ited degree.  Exercise  and  diet  must  be  governed  by  the  same  rules 
that  apply  to  the  more  severe  cases,  although  as  time  progresses 
and  the  heart  appears  to  gain  strength  these  restrictions  do  not 
need  to  be  so  rigorously  enforced.  The  patient  should  be  made  to 
understand,  however,  that  upon  his  obedience  to  the  physician's  in- 
structions, and  his  care  in  avoiding  unwise  effort  as  well  as  ex- 
cesses in  eating  or  any  other  kind,  depends  his  hope  of  prolonging 
life.  In  such  cases  more  depends  upon  habit  and  daily  routine 
than  upon  remedies.  It  is  often  interesting  to  observe  how  true  it 
is  that  these  patients  can  only  learn  by  personal  experience  the 
wisdom  which  their  physician  has  vainly  tried  to  teach  them. 
They  may  be  repeatedly  and  emphatically  warned  against  infrac- 
tion of  rules  of  diet  and  exercise,  lest  they  thereby  bring  on  a 
paroxysm  of  angina  pectoris,  or  aggravate  the  already  existing 
dyspnoea,  and  yet  so  soon  as  symptoms  that  serve  as  a  monitor 
have  become  lessened,  they  think  they  can  allow  themselves  more 
latitude  and  commit  some  indiscretion. 

A  speedy  return  of  angina  or  cardiac  asthma  brings  them  to 
their  senses,  and  they  are  again  ready  to  submit  to  any  restriction. 
The  going  and  coming  of  these  patients  must  be  ordered  by  their 
medical  adviser,  who  therefore  should  keep  them  under  surveil- 
lance that  he  may  discover  early  signs  of  impending  trouble,  and 
take  prompt  action  accordingly. 

Attacks  of  cardiac  asthma  are  most  surely  and  quickly  allevi- 
ated by  hypodermic  injections  of  -J  of  a  grain  of  morphine 
combined  with  ^^o  of  atropine.  A  prompt  effect  is  more  surely 
obtained  by  throwing  the  medicine  into  the  arm  instead  of  the 
leg.  "JMie  relief  thus  afforded  is  sometimes  almost  miraculous 
within  a  few  minutes,  the  patient  being  able  to  lie  down  and  fall 
into  a  refreshing  slnndier.  In  the  less  severe  forms  of  cardiac 
asthma  tlu;  administration  of  the  mor]>hine  at  10  or  11  p.  m.  will 
often   carry   the   sufferer   through   the  night   without  one  of  his 


CHRONIC  MYOCARDITIS  563 

dreaded  attacks.  The  remedy  is  never  so  efficiently  administered 
in  any  other  way  as  under  the  skin,  and  the  dose  should  be  as 
small  as  will  produce  the  desired  effect.  This  will  rarely  be  less 
than  ^  of  a  grain,  which  dose  should  be  administered  nightly  with- 
out increase.  Should  it  be  thought  best  for  any  reason  to  with- 
hold this  remedy,  then  insomnia  may  be  overcome  by  paralde- 
hyde, chloralamide,  and  bromide  together,  or  by  sulphonal. 

The  treatment  of  cardiac  asthma  is  of  a  necessity  that  of  the 
paroxysm  and  the  protection  of  the  patient  against  influences 
which  may  precipitate  an  attack.  If  Cohnheim's  explanation  of 
its  mode  of  production  is  correct — namely,  that  it  is  the  result  of 
temporary  increase  of  left-ventricle  weakness,  in  consequence  of 
which  its  systoles  are  relatively  feebler  than  those  of  the  right — 
then  efforts  must  be  directed  to  the  protection  of  the  degenerated 
left  heart  against  conditions  which  by  raising  arterial  tension 
tend  to  overj)Ower  the  left  ventricle.  Blood-pressure  may  be  in- 
juriously raised  by  the  horizontal  position  of  sleep  without  other 
factors,  and  the  augmentation  of  peripheral  resistance  thus  in- 
duced serves  to  overstrain  this  relatively  too  weak  portion  of  the 
heart.  We  cannot  abolish  the  need  for  sleep,  nor  can  the  patient 
be  required  to  pass  his  nights  in  an  easy  chair,  but  we  can  guard 
him  against  other  harmful  influences,  as  constipation  and  flatulent 
distention  of  the  bowels.  The  former  raises  blood-pressure  in  the 
aortic  system ;  and  the  latter  exerts  injurious  pressure  upon  the 
weakened  heart. 

Dropsy  is  to  be  combated  in  the  usual  way,  by  an  infusion  of 
digitalis  or  diuretin-Knoll,  as  laid  down  in  the  treatment  of 
oedema  from  valvular  disease. 

The  physician  is  not  infrequently  called  to  see  a  patient  suf- 
fering from  excessive  distention  of  the  right  heart,  consequent  it 
may  be  upon  the  rapid  giving  way  of  hypertrophy.  Two  lines  of 
treatment  are  open  to  him :  a  resort  of  free  catharsis  by  some  one 
of  the  drastic  purgatives,  as  elaterium,  or  to  venesection.  There 
is  no  doubt  of  the  speedy  relief  often  following  the  abstraction 
of  16  to  20  ounces  of  blood  from  the  arm,  and  if  the  urgency  of 
the  symptoms  or  the  patient's  exhaustion  make  the  medical  man 
hesitate  to  administer  a  drastic  cathartic,  no  objection  can  be 
urged  against  the  opening  of  a  vein  and  the  letting  of  blood. 
The  relief  thus  afforded  is  justification  enough  for  the  procedure. 


564  DISEASES   OF   THE   HEART 

Moreover,  this  operation  can  then  be  followed  by  the  administra- 
tion of  elateriuni,  jalap,  or  any  other  hydragogue  cathartic. 

In  a  case  of  extreme  dilatation  of  the  heart,  seen  for  the  first 
time  it  may  be,  in  this  dire  condition,  the  administration  of  large 
doses  of  digitalis,  before  having  depleted  the  heart  and  venous 
system  by  venesection  or  hydragogue  catharsis,  is  bad  'practice. 
Thus  overdistended,  the  heart  cannot  respond  to  the  drug  and  only 
struggles  vainly  to  perform  its  work,  like  the  poor  horse  that  in 
response  to  blows  strives  in  vain  to  draw  the  too  heavy  load  up 
hill.  So  it  is  with  the  overburdened  heart.  It  may  be  better  in 
some  cases  to  administer  diffusible  stimulants,  as  ammonia,  cam- 
phor, ether,  and  the  like,  before  })rescribing  digitalis,  and  only 
order  the  latter  after  the  pulse  has  been  improved  in  strength  and 
volume  by  ammonia,  etc. 

Dropsical  accumulation  in  the  serous  cavities  may  be  with- 
drawn by  aspiration,  often  to  the  relief  of  the  sufferer.  Such  a 
l)roeedure  is  of  course  not  calculated  to  help  permanently;  it 
may,  however,  by  lessening  pressure  for  a  short  time,  enable  the 
heart  to  respond  to  stimulation.  When  at  length  all  measures 
have  been  tried  and  found  of  no  permanent  benefit,  the  medical 
attendant  nuiy  then  resort  to  opium  in  some  one  of  its  many  forms 
to  lessen  the  patient's  sufferings.  If  we  cannot  promote  restora- 
tion to  health,  we  are  justified  in  producing  euthanasia.  It  is  a 
physician's  duty  to  prolong  life,  I  presume;  but  I  have  seen  pa- 
tients kept  alive  for  days  by  drugs  when  it  seemed  to  me  it  would 
have  been  far  kinder  not  to  prolong  the  struggle  after  it  became 
manifest  that  the  end  was  not  far  off. 


CHAPTER    XXI 
HYPERTROPHY    OF    THE    HEART 

Morbid  Anatomy. — In  hypertrophy  the  heart-muscle  is  in- 
creased in  thickness  and  weight.  Hypertrophy  of  the  organ  as  a 
whole  is  judged  hy  its  weight,  while  that  of  a  single  chamher  is 
better  estimated  by  a  measurement  of  the  thickness  of  its  walls. 
This  increase  in  size  seems,  according  to  the  latest  investigations, 
to  be  dependent  on  an  increase  in  the  size  of  the  individual  mus- 
cle-fibres. According  to  Gutch,  the  increase  in  breadth  of  the 
fibres  is  insufficient  to  account  for  the  total  increase  in-  weight  of 
the  organ.  He  thinks,  therefore,  that  the  discrepancy  can  be  ex- 
plained by  taking  into  consideration  the  increase  in  interstitial 
fibrous  tissue  that  is  almost  always  present  in  hypertrophied 
hearts,  and  also  by  the  supposition  that  there  is,  with  the  increase 
in  width  of  the  fibre,  a  corresponding  increase  in  length.  These 
two  factors  he  considers  sufficient  to  account  for  the  increase  with- 
out supposing  any  numerical  increase  in  the  fibres,  and  indeed 
evidence  of  the  latter  is  wanting.  The  question  can,  however, 
hardly  be  considered  settled  as  yet. 

The  hypertrophied  muscle  is  firm,  cuts  with  increased  resist- 
ance, and  is  usually  of  a  deep-red  colour.  Increase  of  muscular 
tissue  without  any  corresponding  increase  in  the  blood-supply 
causes  retrograde  changes  to  be  common  in  hypertrophied  hearts, 
and  in  consequence  yellowish  streaks  of  fatty  degeneration,  or 
gray  or  whitish  areas  of  local  fibrosis,  are  not  uncommon.  This 
is  seen  especially  in  the  hypertrophy  accompanying  arteriosclero- 
sis and  renal  disease,  in  which  affections  the  blood-supply  to  the 
myocardium  may  be  reduced  by  reason  of  narrowing  of  the  coro- 
nary vessels. 

The  normal  heart  weighs  about  300  grammes  (10  ounces)  in 
the  male  and  250  grammes  (8.5  ounces)  in  the  female.     These 

565 


h 


HYPERTROPHY  OP  THE  HEART  567 

figures  are  for  individuals  of  the  average  size,  but  of  course  the 
heart  weight  varies  with  that  of  the  whole  body.  In  hypertrophy 
the  weight  may  be  doubled  or  even  tripled.  Stokes  is  said  to 
have  reported  a  heart  weighing  60  ounces,  but  one  weighing  more 
than  000  grammes  (20  ounces)  is  a  very  large  organ.  According 
to  Eichhorst,  a  generally  enlarged  heart  may  attain  such  dimen- 
sions as  to  extend  from  the  right  mamillary  to  the  left  midaxil- 
lary  line.  When  the  left  ventricle  is  chiefly  involved  the  organ 
is  conical  and  its  apex  blunt  and  broad  (Fig.  lO-i).  When  the 
right  chamber  is  also  enlarged  it  assumes  a  more  quadrangular 
form,  and  the  apex  is  formed  wholly  by  the  right  ventricle 
(Plate  III). 

The  papillary  muscles  and  columnge  earner  share  in  the  gen- 
eral hypertrophy,  the  latter  especially  in  the  right  chamber 
(Osier).  Hypertrophy  may  be  circumscribed,  however,  and  then 
the  trabecular,  papillary  muscles,  either  conus,  or  one  of  the  au- 
ricular appendices,  may  be  the  seat  of  the  change.  Such  local 
hypertrophy  is  not  common  and  probably  is  due  to  trophic  changes 
rather  than  to  any  circulatory  disturbances. 

Post-mortem  rigidity  of  the  heart-muscle  may  simulate  hyper- 
trophy by  causing  the  heart-wall  to  be  thicker  than  normal,  and 
hence  increase  in  weight  is  the  only  trustworthy  sign. 

Concentric  hypertrophy,  or  thickening  of  the  wall  of  a  cham- 
ber without  increase  in  its  capacity,  is  but  rarely  met  with  (Fig. 
10).  It  is  usually  the  result  of  stenosis.  Hypertrophy  combined 
with  more  or  less  dilatation  of  the  chamber — i.  e.,  eccentric  hyper- 
trophy— is  by  far  the  more  usual  condition.  When  such  a  heart 
comes  to  autopsy,  the  dilatation  has,  as  a  rule,  broken  down  the 
hypertrophy  and  is  the  predominating  feature. 

For  the  purposes  of  comparison,  I  give  the  following  figures, 
quoted  by  Eichhorst,  from  Thoma's  tables : 

Weight  of  Heart 

Until  the  end  of  the  first  year 37  grammes. 

Second  to  fifth  year 50  to    70 

Sixth  to  tenth  year 70  to  115 

Eleventh  to  fifteenth  year 130  to  205 

Sixteenth  to  twentieth  year 218  to  254 

Twenty-first  to  thirtieth  year 260  to  294 

Thirty-first  to  fiftieth  year 297  to  308 

Fiftieth  to  sixty-fifth  year 308  to  332 

Sixty-fifth  to  eighty-fifth  year 832  to  303 


568  DISEASES   OF  THE   HEART 

Eichliorst  also  furnishes  the  foHowing  table  from  Bizot 


In  males. 


Length  of  tlic  heart  ....    

Widtli  of  tlie  heart 

Thickness  of  tlie  heart 

Thickness  of  the  left  ventricle  at  the  base 

Thickness  of  the  left  ventricle  at  the  middle 

Thickness  of  the  right  ventricle  at  the  base 

Thickness  of  the  right  ventricle  at  the  middle 

Thickness  of  the  right  ventricle  at  the  apex 

Thickness  of  the  sa^ptum  ventriculorum  at  the  middle.. 


Millimetres. 

85  to    90 

93  to  105 

30  to    35 

10.1 

11.6 

4.5 

3.1 

2.5 

11.0 


In  females. 

Millimetres. 

80  to  85 
85  to  92 
30  to  35 

9.8 
10.8 

3.7 

2.8 

2.1 

9.0 


Etiology. — Hypertrophy  of  the  heart  is  rarely  met  with 
clinically  except  as  secondary  to  some  other  condition.  Thus  we 
have  seen  that  it  is  a  part  of  the  process  styled  chronic  myocar- 
ditis, and  is  present  also  in  valvular  disease  and  adherent  peri- 
cardium. It  is  often,  though  not  necessarily,  associated  with 
arteriosclerosis.  These  affections  may  all  he  ranked  among  its 
etiological  factors,  but,  as  it  is  not  of  hypertrophy  thus  occasioned 
that  I  intend  now  to  speak,  they  may  be  dismissed  with  this  bare 
mention. 

liypertroi)liy  of  the  whole  heart,  but  chiefly  of  the  left  ventri- 
cle, is  an  almost  invariable  sequel  to  chronic  disease  of  the  kidneys, 
especially  of  interstitial  nephritis,  although  also  of  the  chronic 
parenchymatous  variety  and,  according  to  Fraentzel,  of  long- 
standing pyelonephritis.  There  is  persistently  high  pulse-tension 
in  these  cases,  but  there  is  probably  some  additional  influence  at 
work  in  the  production  of  the  hypertrophy — to-xtrmia,  it  may  be, 
or  atheroma.  Cardiac  hypertroi)hy  of  this  origin  becomes  a  clini- 
cal entity  only  as  it  is  incidentally  discovered  in  connection  with 
the  nephritis  or  after  indications  of  myocardial  inadequacy  have 
declared  themselves. 

A  much  less  frecpiont  but  by  no  ineaus  unimportant  cause  of 
]iy])(ifi-(iphy  of  th(^  left  ventricle  is  congenital  smallness  of  the 
aorta  or  of  the  entire  arterial  system.  There  is  usually  some 
otlier  abnormality,  as  persistence  of  Botalli's  duct,  whenever  the 
narrowing  is  limited  to  the  isthmus  of  the  aorta  or  is  extreme;  but 
ill  minor  degrees  of  narrowing  an  increase  in  the  thickness  of  the 
heart-wall  is  the  only  result.  This  condition  is  not  unimportant, 
for,  according  to  German  authors,  it  leads  to  cardiac  incompe- 


HYPERTROPflY  OF   THE   HEART  569 

tence  and  dilatation  in  young  soldiers  who  arc  subjected  to  the 
strain  of  long,  toilsome  marches. 

In  chronic  Bright's  disease  and  congenital  smallness  of  the 
aorta,  hypertrophy  develops  in  consequence  of  abnormal  periph- 
eral resistance,  which  forces  the  heart-muscle  to  perform  extra 
work.  It  therefore  becomes  increased  in  size  (see  Morbid  Anat- 
omy), the  same  as  does  a  skeletal  muscle  under  like  conditions. 
Yet  the  muscular  fibres  could  not  grow  in  thickness  and  length 
if  they  did  not  receive  sufficient  nourishment,  and  hence  aug- 
mented nutritive  supply  is  indispensable.  It  is  this  consideration 
which  leads  German  writers  to  regard  the  consumption  of  inordi- 
nate quantities  of  beer  as  an  undoubted  cause  of  the  enormous 
hearts  seen  among  excessive  beer-drinkers  of  Bavaria.  The  intake 
of  large  amounts  of  fluid  alone  would  not  be  capable  of  producing 
cardiac  hypertrophy,  no  matter  how  greatly  they  increase  periph- 
eral resistance,  but  containing  no  inconsiderable  proportion  of 
nutritive  elements,  as  it  does,  the  excessive  consumption  of  beer 
furnishes  all  the  requisites  for  the  causation  of  hypertrophy. 

It  is  believed  that  contestants  for  athletic  honours,  particu- 
larly oarsmen  and  professional  bicyclists,  develop  this  form  of 
heart-disease,  and  doubtless  some  of  them  do.  The  hypertrophy  is 
thought  to  result  from  the  heart  having  to  overcome  abnormal  pe- 
ripheral resistance  created  by  severe  muscular  effort.  This  is  not 
the  correct  explanation,  since  the  initial  rise  of  blood-pressure  oc- 
casioned by  muscular  contraction  is  later  on  followed  by  a  fall  as 
the  intermuscular  arterioles  become  dilated.  Therefore  some 
other  factor  is  responsible  for  the  hypertrophy.  This  may  lie  in 
some  unrecognised  abnormality  of  the  vascular  system,  but  in  the 
case  of  professional  wheelmen  and  rowers  is  probably  due  to  the 
constrained  position  they  take  during  their  exertions.  As  seen  in 
the  next  chapter,  the  heart-strain  of  athletic  contests  is  much  more 
likely  to  result  in  dilatation. 

In  the  case  of  soldiers,  mountaineers,  peddlers,  labourers,  or 
others  who  carry  heavy  packs  stra2")ped  on  their  shoulders,  the  in- 
jurious effect  on  the  heart  is  to  be  attributed  to  the  combined  influ- 
ence of  respiratory  embarrassment  and  arduous  physical  exertion, 
even  granting  that  there  are  no  such  influences  at  work  as  abuse 
of  alcohol,  atheroma,  etc. 

Rapid  and  violent  action  of  the  heart  of  a  psychical  origin  is 


570  DISEASES  OF  THE  HEART 

also  thought  to  produce  hypertroj^hy,  but  it  is  likely  that  tachy- 
cardia and  palpitation  alone  are  incapable  of  such  a  result.  The 
hypertrophy  and  dilatation  of  the  heart  observed  in  exophthalmic 
goitre  is  to  be  attributed  not  to  tachycardia  but  to  the  underlying 
condition,  whatever  that  may  be. 

Hypertrophy  of  the  right  ventricle  is  a  sequel  of  various  tho- 
racic disorders — i.  e.,  pulmonary  emphysema,  cirrhosis  of  the 
lungs,  pleuropericardial  adhesions  and  chest  deformity,  as 
kyphoscoliosis.  In  these  conditions  there  is  excessive  peripheral 
resistance  in  the  lesser  circulation  from  compression  or  even  oblit- 
eration of  pulmonary  capillaries.  In  time,  as  the  nutrition  of  the 
heart  suffers,  its  undue  strain  leads  to  dilatation  and  even  to  de- 
generation. 

A  so-called  physiological  hypertrophy  of  the  left  ventricle  is 
said,  especially  by  the  French,  to  take  place  during  pregnancy. 
There  probably  does  develop  an  increased  weight  of  the  heart,  a 
true  hypertrophy  of  the  muscle-fibres,  but  it  is  never  so  consider- 
able as  to  become  of  clinical  importance. 

To  sum  up :  As  remarked  by  Krehl,  the  development  of  hyper- 
trophy has  to  do  essentially  with  the  propulsion  of  an  increased 
volume  of  blood,  with  the  overcoming  of  abnormal  resistance,  or 
with  a  union  of  both  these  factors,  and.  each  one  of  them  may 
depend  upon  a  variety  of  causes. 

Symptoms. — Hypertrophy  of  the  heart  is  to  be  regarded  as 
a  wise  provision  on  the  part  of  Nature  by  which  the  organ  is 
enabled  not  alone  to  perform  increased  work  but  to  accommodate 
itself  to  those  conditions  which  render  increased  work  necessary. 
The  normal  heart  can  perform  increased  labour  by  putting  forth 
extra  exertion,  but  its  ability  in  this  direction  is  limited.  If, 
therefore,  the  heart  did  not  respond  to  demands  for  extra  effort 
by  the  development  of  hypertrophy,  its  accommodative  power  to 
diseased  conditions  would  soon  reach  its  limit.  Consequently  car- 
diac hypertrophy  may  be  regarded  as  a  conservative  process. 

These  considerations  make  it  a])parent  that  there  are  no  symp- 
toms directly  referable  to  hyj)ertr()])liy  of  the  heart  as  such.  If 
tachycardia,  attacks  of  palpitation,  and  irregular  or  intermittent 
action  of  the  organ  disturb  the  patient,  they  are  not  due  to  the 
increase  in  its  size  but  to  disturbing  conditions  without,  or  are  to 
be  regarded  as  an  indication  of  beginning  inadequacy.     In  other 


HYPERTROPHY   OP  THE  HEART  571 

words,  tlu;  extra  labour  required  of  the  lieart  is  beginning  to  tell 
on  it,  and  if  the  undue  strain  is  continue<l,  its  reserve  strength 
will  become  exhausted.  The  hypertrophy  is  discovered  either 
accidentally  or  because  a  supervening  dilatation  occasions  sub- 
jective sensations  which  bring  the  individual  to  the  physician. 

Physical  Signs. — Insijcction. — The  amount  of  information 
derived  from  ins})ection  of  the  patient  depends  upon  the  degree 
of  hypertrophy  and  conditions  residing  in  the  thoracic  walls  and 
lungs.  If  the  chest  is  capacious  and  the  lungs  are  interposed 
between  the  chest-wall  ai^d  heart,  there  may  be  no  visible  impulse. 
When,  on  the  contrary,  the  parietes  are  thin  and  the  organ  is  con- 
siderably enlarged,  it  produces  visible  shock  which  is  exaggerated 
both  in  force  and  extent,  while  the  apex-beat  is  displaced  outward 
and  in  some  instances  downward,  according  to  the  degree  of 
hypertrophy.  In  hypertrophy  of  the  right  ventricle  there  is  apt 
to  be  visible  pulsation  in  the  epigastrium. 

Palpation. — Confirmation  of  the  facts  perceived  by  the  eye  is 
obtained  by  the  hand,  and  for  the  most  part  nothing  more.  In 
some  instances  careful  palpation  enables  one  to  locate  the  position 
of  the  apex-beat  when  this  is  not  visible,  and  to  judge  of  the  force 
and  extent  of  cardiac  contractions.  In  women  with  large  mam- 
mary development  in  whom  inspection  and  percussion  are  futile, 
palpation  is  often  of  great  aid  in  estimating  the  size  of  the  organ. 
The  pulse  of  left-ventricle  hypertrophy  is  full,  strong,  and  in- 
clined to  be  slow  rather  than  accelerated.  Increase  in  its  rate 
comes  on,  as  a  rule,  only  when  dilatation  begins  to  gain  ascend- 
ency and  cardiac  insufficiency  to  declare  itself.  It  is  a  pulse  of 
high  and  sustained  tension,  as  shown  by  pressure  of  the  finger  on 
the  artery  and  by  Gaertner's  tonometer  or  the  sphygmograph. 
This  is  not  due  to  stiffness  of  the  vascular  coats,  but  to  the  in- 
creased force  with  which  the  blood-wave  is  propelled  by  the  power- 
fully contracting  ventricle.  Such  a  pulse  is  difficult  to  compress, 
but  when  the  artery  has  been  thus  collapsed,  the  wave  of  blood  is 
felt  to  strike  the  palpating  finger  strongly,  while  below  the  point 
of  pressure  the  vessel  is  empty  and  its  coats  cannot  be  rolled  be- 
neath the  finger,  showing  that  they  are  not  thickened  and  the  in- 
crease of  tension  is  not  due  to  atheroma. 

Percussion. — This  forms  our  best  and  most  reliable  means  of 
determining  increase  in  the  size  of  the  heart.     Absolute  dulness 


572  DISEASES  OP  THE  HEART 

may  not  be  greater  than  normal,  but  the  relative  is,  as  sho^vn  by 
some  one  of  the  various  modes  of  i)ercussion  described  in  the 
introductory  chapter.  Increase  of  deep-seated  dulness  to  the 
left  and  upward  is  indicative  of  left-ventricle  hypertrophy,  pro- 
vided, of  course,  the  organ  is  not  displaced. 

The  measurements  given  in  the  article  on  chronic  myocarditis 
show  that  the  distance  between  the  midsternum  and  left  nipple 
is  not  constant  in  all  persons,  but  varies  within  considerable  limits. 
It  is  not  safe,  therefore,  to  conclude  that  because  relative  dulness 
does  not  pass  outside  the  nipple  the  heart  is  of  normal  size,  yet,  if 
dulness  is  found  to  extend  beyond  the  vertical  nipple-line,  it  is 
pretty  sure  evidence  that  hypertrophy  exists.  Likewise  an  in- 
crease of  relative  dulness  to  the  right  and  downward  betokens 
hypertrophy  of  the  right  ventricle.  The  measurements  for  the 
normal  heart  may  be  found  in  the  introductory  chapter. 

Auscultation. — As  one  of  the  elements  entering  into  the  pro- 
duction of  the  first  heart-sound  is  the  muscular  element,  or  that 
produced  by  the  contraction  of  the  wall  and  papillary  muscles,  the 
first  sound  is  generally  loud  and  booming.  It  is  also  apt  to  be 
rather  prolonged.  A  more  reliable  criterion  is  obtained,  however, 
by  the  study  of  the  second  sound  at  the  base.  Owing  to  the  high 
pulse  tension  present  in  left-ventricle  hypertrophy,  the  aortic 
second  tone  is  accentuated,  and  this  intensification  is  generally  put 
down  as  one  of  the  signs  of  hypertrophy.  It  is  only  of  value, 
however,  in  connection  with  other  signs.  Similarly  accentuation 
of  the  pulmonic  second  sound  is  an  auscultatory  sign  of  hyper- 
trophy of  the  right  ventricle.  It  should  be  remembered,  however, 
that  in  children  and  young  adults  this  tone  is  normally  louder 
than  the  aortic.  Auscultation  is  a  much  less  reliable  means  of 
judging  of  the  size  of  the  heart  than  is  percussion,  since  various 
conditions  may  temporarily  alter  the  relative  intensity  of  the 
sounds. 

Diagnosis. — The  recognition  of  cardiac  hypertrophy  de- 
pends not  alone  upon  its  degree,  but  also  upon  various  conditions 
on  the  part  of  the  lungs  and  thoracic  parietes.  Minor  degrees 
may  be  assumed  but  cannot  always  be  made  out  with  certainty. 
On  the  other  hand,  a  heart  may  be  greatly  hypertrophied  and  yet 
may  escape  our  recognition  because  it  is  covered  over  by  a  volumi- 
nous or  emphysematous  lung,  or  the  chest-wall  may  be  so  thick 


HYPERTROPHY  OP  THE  HEART  573 

from  fat  and  muscle  as  to  render  ordinary  methods  of  diagnosis 
futile. 

The  clinical  findings  generally  thought  to  warrant  a  diagnosis 
of  cardiac  hypertrophy  are:  (1)  A  full,  tense  pulse  which  is  either 
slow  or  of  normal  rate,  not  accelerated;  (2)  a  powerful,  broad 
apex-beat  which  is  displaced  outward  and  perhaps  downward;  (3) 
increased  cardiac  dulness  to  the  left  and  upward  or,  it  may  be,  in 
all  diameters;  (4)  a  booming,  low-pitched  first  sound  and  an  ac- 
centuated aortic  second  sound.  Hypertrophy  of  the  right  ventri- 
cle is  shown  by:  (1)  Epigastric  pulsation,  (2)  increase  of  cardiac 
dulness  to  the  right  and  downward,  and  (3)  intensification  of  the 
pulmonic  second  tone.  Should  the  condition  of  the  lungs  or 
thoracic  walls  not  enable  one  to  rely  on  the  evidence  furnished  by 
the  usual  means  of  physical  examination,  then  one  may  have  re- 
course to  the  fluoroscope,  which  ought  to  settle  the  diagnosis 
beyond  further  question. 

Differential  Diagnosis. — It  is  hardly  necessary  to  remind  the 
reader  that  displacement  of  the  heart  towards  either  side  may 
simulate  hypertrophy,  and  therefore  must  be  excluded.  The  most 
frequent  source  of  error  in  this  direction,  however,  lies  in  the  fact 
that  scoliosis,  or  that  forward  curvature  of  the  spinal  column,  may 
cause  the  heart  to  lie  close  against  the  anterior  chest-wall  and  to 
pulsate  so  forcibly  and  widely  as  to  give  an  appearance  of  marked 
hypertrophy.  In  all  cases,  therefore,  the  shape  and  depth  of  the 
thorax  ought  to  be  carefully  scrutinized. 

In  addition,  I  wish  to  refer  to  what  Italian  writers  term 
"  pseudo-cardiac  hypertrophy,"  by  which  is  meant  a  condition 
sometimes  observed  in  young  persons  who  are  neurotic  and  have 
thin  chest-walls  with  broad  intercostal  spaces.  In  such,  owing  to 
excitability,  the  action  of  the  heart  is  apt  to  be  rapid  and  unduly 
forcible.  The  apex  of  the  organ  strikes  in  the  broad  and  thin 
intercostal  space  with  what  appears  to  be  exaggerated  force  and 
abnormal  breadth,  or  the  entire  cardiac  area  may  heave  strongly 
with  each  systole.  The  heart-sounds  are  intensified  and  ringing, 
and  altogether  the  organ  conveys  the  impression  of  abnormal 
strength.  Consequently,  unless  the  examiner  makes  careful  meas- 
urements of  deep-seated  dulness,  he  is  very  liable  to  erroneously 
conclude  that  he  has  to  do  with  a  hypertrophied  heart. 

In  all  cases  in  which  hypertrophy  is  suspected  and  physical 


574  DISEASES  OP  THE  HEART 

signs  are  not  eunvincing,  a  positive  diagnosis  of  the  affection 
should  not  be  made  until  some  condition  has  been  discovered 
which  is  capable  of  inducing  hypertrophy.  In  the  absence  of  such 
predisposing  conditions  hypertrophy  is  not  likely  to  occur,  and 
hence  one  should  be  conservative  in  relying  on  physical  signs  if 
they  are  not  very  conclusive. 

The  liability  to  error  was  forcibly  impressed  upon  me  by  the 
case  of  a  young  coloured  man  who  was  an  applicant  for  life  insur-- 
ance  and  who  was  likely  to  be  rejected  by  the  examiner  because  of 
a  supposed  enlargement  of  the  right  ventricle.  Absolute  cardiac 
dulness  was  manifestly  increased  transversely,  whereas  relative 
dulness  as  shown  by  careful  measurement  was  not  augmented.  It 
was  then  noted  that  he  stood  in  a  very  faulty  attitude  with  his 
shoulders  thrown  strongly  backward  and  the  scapula  pressed 
closely  against  each  other.  In  this  position  the  spinal  colunm  was 
forced  strongly  forward  to  such  an  extent  that  it  shortened  the 
antero-posterior  diameter  of  the  thorax,  and  consequently  pressed 
the  heart  against  the  anterior  chest-wall  so  as  to  crowd  the  lung- 
borders  aside  and  produce  an  apparent  enlargement  of  the  heart. 

In  some  instances  the  diagnosis  of  cardiac  hypertrophy  is 
made  almost  at  a  glance,  but  in  minor  degrees  its  determination 
is  only  possible  after  one  has  carefully  considered  the  degree  of 
blood-pressure. 

For  the  differential  diagnosis  of  hypertrophy  from  dilatation 
the  reader  is  referred  to  the  succeeding  chapter. 

Prognosis. — The  prognosis  of  the  condition  we  are  now  con- 
sidering may  be  said  to  be  that  of  its  cause.  If  this  is  of  a  pro- 
gressive nature  so  that  it  is  only  a  question  of  time  when  peri])h- 
eral  resistance  will  outstrip  the  accommodative  ability  of  the 
heart,  prognosis  is  ultimately  unfavourable.  It  should  be  borne 
in  mind,  moreover,  that  the  hypertrophied  heart-muscle  is  likely 
to  suffer  degeneration;  and  wlicn  this  sets  in  cardiac  inadequacy  is 
ultimately  inevitable.  If  hypertr()])hy  of  the  left  ventricle  is  asso- 
ciated with  a  granular  kidney  and  vascular  changes,  ])rognosis  is 
influenced  by  the  possibility  of  rupture  of  a  brittle  cerebral 
artery. 

If  hypertrophy  has  resulted  from  the  abuse  of  athletic  sports 
and  the  individual  is  still  young,  with  healthy  vessels,  the  condi- 
tion may  not  prove  serious  providing  the  exciting  cause  is  re- 


HYPERTROPHY  OF   THE   HEART  575 

moved.  In  such  persons,  however,  one  should  not  ignore  the  pos- 
sibility of  congenital  smallness  of  the  arterial  system. 

Treatment. — Hypertrophy  of  the  heart  does  not  require 
therapeutic  interference,  and  hence  one  should  not  attempt  to 
lessen  the  vigour  of  cardiac  contractions,  as  I  have  known  at- 
tempted, by  the  use  of  aconite.  The  increased  thickness  of  the 
heart-wall  is  a  conservative  measure.  The  aim  should  rather  be 
to  preserve  hypertrophy  and  protect  the  heart  from  the  inadequacy 
of  overstrain.  The  underlying  condition  is  the  object  of  our  solici- 
tude. Valvular  lesions,  pericardial  adhesions,  chronic  nephritis, 
congenital  smallness  of  the  aorta — these  and  many  other  causes 
cannot  be  removed.  When  detected,  their  existence  should  be 
stated  to  the  patient  and  he  should  be  warned  against  the  danger 
of  breaking  down  his  hypertrophy  by  unwise  physical  efforts  or 
any  other  injurious  influences.  If  the  cause  lies  in  the  excessive 
consumption  of  beer,  in  gluttony,  in  faulty  athletic  exercise,  the 
patient  should  be  plainly  informed  of  his  injurious  practices  and 
urged  to  desist  before  they  lead  to  cardiac  insufficiency. 

If  disordered  action  of  the  heart  seems  to  call  for  digitalis; 
this  remedy  should  be  administered  with  great  caution.  As  a 
matter  of  fact,  such  an  invigorator  of  cardiac  systole  is  not  indi- 
cated unless  signs  of  myocardial  incompetence  are  actually  pres- 
ent. When  this  is  the  case  it  is  no  longer  the  hypertrophy  but  it 
is  the  dilatation  which  calls  for  treatment.  This  will  be  found 
detailed  in  the  appropriate  place. 


CHAPTER    XXII 

DILATATION    OF    THE    HEART— RELATIVE    AND 
MUSCULAR    MITRAL    INSUFFICIENCY 

I.  DILATATION   OF  THE    HEART 

Except  in  cases  of  acute  overdistention,  dilatation  of  the 
heart  is  rarely  primary,  but  secondary  to  some  affection  of  an 
acute  or  chronic  nature,  as  pericarditis,  acute  and  chronic  myo- 
carditis, and  valvular  disease,  and  the  diagnosis  should  not  be 
made  merely  of  dilatation,  but,  if  possible,  of  the  underlying 
pathological  etiological  condition.  These  have  been  already  con- 
sidered in  previous  chapters,  and  to  them  the  reader  is  referred 
for  particulars.  More  or  less  dilatation  of  the  heart  is  recognis- 
able whenever  there  is  cardiac  incompetence  from  whatever  cause, 
but  in  this  ehai)ter  the  endeavour  will  be  made  to  ])ortray  what 
may  be  considered  as  overstrain  of  the  heart-walls,  whether  grad- 
ually or  acutely  induced,  and  independent  of  previous  recognis- 
al^le  myoeai'dial  or  endocardial  disease. 

Morbid  Anatomy. — By  dilatation  of  the  heart  is  meant  an 
increase  in  llie  caj)a('ity  of  its  chambers  due  to  rapid  or  gradual 
stretching  of  its  Avails.  In  most  cases  hypertrophy  is  combined 
with  dilatation  and  has  preceded  tlie  development  of  the  latter. 
A  dilated  heart  is  as  hirge  or  larger  than  one  only  hypertrophied, 
but  the  muscl(!  is  flabby,  and  the  organ  does  not  keep  its  slia])e 
when  laid  on  tlie  table.  Extreme  instances  have  been  described 
in  wliicli  tlie  heart  held  up  by  the  great  vessels  collapsed  over  the 
hand  so  as  to  cover  it  like  a  mushroom.  This  flabbiness  is  not 
characteristic  of  dilatation  as  such,  but  of  all  conditions  of  the 
myocardiiiiii  in  which  tlie  nniscde  lias  lost  its  tone  and  Avhich  have 
predisposed  the  organ  to  stretching.  'I'hese  are  cloudy  swelling, 
fatty  degeneration,  etc.  ■  Slight  d(!grees  of  dilatation,  as  well  as 
acute  overstrain,  are  not  attended  by  these  myocardial  changes — 
576 


■  V  i  fejt 


EXTEEIOE  OF  HEAET  OF   FIG.   42.   SHOWING   HYPEETEOPHY  AND 
DILATATION  OF   BOTH   VENTEICLES. 


dilatatio'n  of  the  heart  577 

tBey  are  often  a  part  of  the  compensatory  process  attending  valvu- 
lar lesions.  When,  however,  compensation  breaks  down  and  dila- 
tation becomes  extreme,  the  walls  are  found  degenerated  and 
flabby.  The  muscle  is  usually  paler  than  normal  and  may  be 
cloudy  or  of  a  brownish  tint,  due  to  the  deposit  of  pigment. 

As  dilatation  usually  results  from  the  further  action  of  the 
causes  that  produce  hypertrojDhy,  it  has  much  the  same  distribu- 
tion. It  may  affect  but  one  chamber  or  the  heart  as  a  whole. 
The  trabecule  and  papillary  muscles  are  naturally  not  concerned 
in  the  process  of  dilatation  except  in  so  far  as  the  latter  may 
stretch  or  lengthen  in  order  to  functionate  properly  wdthin  the 
enlarged  chambers.  Relative  insufficiency  of  the  valves  is  gener- 
ally present  and  may  be  caused  by  stretching  of  their  ostia  or  of 
the  cardiac  walls. 

Etiology. ^ — Cardiac  dilatation  may  be  said  to  be  the  result  of 
a  disproportion  between  the  work  the  heart  has  to  do  and  its  abil- 
ity to  do  it.  This  undue  demand  upon  its  energies  may  have  ex- 
isted for  years  in  the  form  of  prolonged  high  arterial  tension, 
and  only  at  length  become  disproportioned  through  degeneration 
and  gradual  waning  of  the  heart-power..  ISTot  infrequently  it  is 
some  unexpected  call  for  extra  effort  that  overpowers  the  heart, 
when  without  it  the  organ  might  have  been  able  to  perform  its 
work  successfully  for  years  longer.  It  is  in  this  way  that  dilata- 
tion so  often  succeeds  compensatory  hypertrophy  in  valvular  dis- 
ease. In  many  but  not  all  such  cases  the  integrity  of  the  heart- 
muscle  has  been  slowly  undermined  by  the  development  of  degen- 
erative changes. 

Such  an  exciting  cause  of  dilatation  may  be  a  hasty  run, 
a  spurt  on  a  bicycle,  the  lifting  or  carrying  of  a  heavy  weight,  a 
prolonged  debauch,  etc.  Anxiety,  grief,  and  even  fright,  through 
their  action  on  the  inhibitory  nerve  of  the  heart,  are  capable  of 
inducing  a  stretching  of  the  cardiac  walls  through  stasis  in  the 
cavities  they  inclose — the  "  stauungs  "  dilatation  of  the  Germans. 

Romberg  lays  stress  on  the  deleterious  influence  in  this  re- 
spect of  acute  infectious  diseases,  and  cites  instances  in  which  he 
has  observed  cardiac  dilatation  and  ultimately  fatal  insufficiency 
follow  an  attack  of  influenza.  I  have  notes  of  the  case  of  a  gentle- 
man of  fifty-seven  wdiose  dilatation  and  eventual  death  from  pro- 
gressive cardiac  asthenia  were  attributable  to  his  having  carried 
38 


578  DISEASES  OP  THE  HEART 

a  heavy  travelling  bag  several  blocks  in  Denver  at  an  altitude  f>f 
5,280  feet.  As  this  patient  was  moderately  corpulent,  weighing 
192  pounds,  his  heart  was  probably  not  sound  at  the  time  of  his 
exertion,  and  yet  it  had  been  adequate  to  all  demands  made  on  it 
previously. 

We  sometimes  observe  dilatation  of  the  heart  when  we  have 
no  reason  to  assume  that  the  organ  is  the  seat  of  wide-spread 
structural  disease  and  there  may  be  no  extensive  post-mortem  al- 
terations that  can  be  recognised.  The  heart-walls  are  soft  and 
flabby,  and  that  is  all  that  can  be  said  of  them.  In  such  a  case  the 
individual  may  have  been  ana-mic,  or  his  heart-muscle  as  well  as 
his  skeletal  muscles  has  been  weakened  by  ycArs  of  close  applica- 
tion to  business  or  intellectual  pursuits.  Without  any  preparation 
such  an  individual  takes  to  bicycling  and  at  once  indulges  in  long 
tours  at  a  scorching  pace  up  hill  and  down,  over  I'ough  sandy  roads 
and  against  heavy  winds.  Under  the  absurd  impression  that  such 
exercise  is  good  for  his  weak  muscles,  he  heeds  not  his  panting 
respirations  and  rapid  heart-beats.  But  outraged  Nature  avenges 
the  insult  by  permitting  the  gradual  if  not  sudden  development  of 
cardiac  dilatation. 

I  once  had  under  treatment  for  a  time  a  clergyman  of  mid- 
dle age  who  had  left-ventricle'  dilatation  with  relative  mitral 
incompetence  as  the  result  of  a  single  injudicious  effort  of  this 
kind.  As  he  expressed  it,  "  he  had  pumped  up  "  the  steepest 
road  on  the  banks  of  the  Hudson  River  a  thousand  feet  up  the  face 
of  the  Palisades — a  road  so  steep  that  very  few  were  ever  able  to 
make  the  ascent  on  their  wheels.  Although  not  aware  of  injury 
at  the  time,  ho  not  long  thereafter  began  to  suffer  from  alarming 
fainting  spells,  the  first  of  which  seized  him  while  delivering  a 
sermon.  Fortunately  for  him  his  heart-muscle  was  sound  and 
ultimately  recovered  its  tone. 

It  is  rather  singular  that  I  have  been  called  on  to  treat  for  car- 
diac incompetence  due  to  dilatation  from  strain  throe  men  whose 
occupations  required  them  to  inspect  buildings  in  the  process  of 
construction.  Failing  to  discover  any  sntisfactory  cause  for  their 
dilatation,  I  was  led  to  inquire  minutely  concerning  possible  heart- 
strain,  and  found  they  were  in  the  habit  of  climbing  ladders  or 
ascending  many  fliglits  of  stairs  in  order  to  reach  tlie  different 
parts  of  tlieir  l)uil(lings.     It  lias  sccnicd  to  me  very  reasonable  to 


DILATATION  OF  THE  HEART  579 

assume  the  likelihood  of  heart-strain  by  such  exertion,  and  in  the 
case  of  one  of  these  men  intermittence  persisted  in  spite  of  treat- 
ment until  he  exchanged  his  work  as  building  inspector  for  a 
sedentary  occupation  in  an  ofSce. 

In  not  a  few  instances  the  resistance  of  the  myocardium  is 
diminished  by  the  inordinate  use  of  tobacco  or  by  sexual  excesses, 
late  hours  and  social  dissipation,  dancing,  etc.  In  one  case  the 
young  man  breaks  down  in  his  nervous  system,  a  second  develops 
a  cough,  while  still  another  manifests  signs  of  cardiac  dilatation 
that  may  have  been  suddenly  or  gradually  induced.  In  most  of 
such  cases  complete  restoration  of  heart-power  follows  removal  of 
the  cause  and  appropriate  treatment.  In  some  the  heart  remains 
permanently  impaired,  and  in  others  every  fresh  excess  is  followed 
by  renewed  dilatation  until  at  length  irreparable  cardiac  stretch- 
ing and  insufficiency  remain.  Such  examples  are  not  confined  to 
the  male  sex. 

Anajmia  and  chlorosis  predispose  to  this  form  of  heart-disease, 
and  more  than  one  society  belle  pays  for  the  season's  round  of 
dancing  and  other  gaiety  by  slowly  or  acutely  induced  incompe- 
tence of  the  dilated  heart.  Many  a  jaded  matron  who  declares  she 
is  "  worn  out "  by  the  demands  of  society  is  really  suffering  from 
serious  though  perhaps  not  extensive  stretching  of  the  heart-cham- 
bers. Her  heart-muscle  has  grown  flabby  and  is  not  always  capa- 
ble of  entire  restoration. 

Fortunately  the  heart-muscle  is  susceptible  of  development  the 
same  as  are  the  voluntary  muscles.  Were  it  not  so,  the  athlete 
would  be  incapable  of  competing  for  the  laurel  wreath  of  victory. 
If,  however,  he  is  overtrained  or  if  his  training  prove  inadequate, 
the  heart  may  be  the  part  that  suffers.  Under  such  circumstances 
acute  dilatation  may  result  from  a  single  contest.  It  usually 
affects  the  right  ventricle,  and  stretching  of  the  right  auriculo-ven- 
tricular  ring  permits  the  "  safety-valve  action  of  the  tricuspid  "  to 
come  into  play.  (See  the  chapter  on  Tricuspid  Regurgitation.) 
It  is  possible,  however,  for  the  left  ventricle  also  to  become  acutely 
overdistended,  as  was  shown  by  cases  reported  by  Harold  Wil- 
liams. 

If  muscular  incompetence  of  these  valves  is  set  up,  then  the 
strain  is  lifted  somewhat  from  the  walls  of  the  left  ventricle  and 
shared  by  those  of  the  left  auricle  and  pulmonary  veins.     This  is 


580  DISEASES   OF   THE   HEART 

likewise  a  compensatory  provision  on  the  part  of  iSTatiirc,  for  with- 
out it  there  would  be  positive  danger  of  diastolic  arrest  of  the 
overtaxed  left  ventricle.  In  carefully  trained  athletes,  or  in  the 
young  with  a  robust  myocardium,  such  a  degree  of  cardiac  strain 
is  usually  recovered  from  s])eedily  and  permanently.  If  the  walls 
are  not  perfectly  sound,  or  if  there  is  sustained  high  blood-pres- 
sure in  the  aortic  system  because  of  vascular  or  renal  disease,  or 
if  the  heart  is  too  frequently  subjected  to  overstrain,  permanent 
dilatation  may  result  with  all  its  consequences. 

Finally  I  desire  here  to  dwell  on  the  harm  in  this  regard  that 
is  likely  to  accrue  to  young  children  from  the  immoderate  use  of 
the  bicycle  and  from  games  that  necessitate  long,  hard  running. 
There  is  actual,  not  fancied,  danger  of  cardiac  dilatation.  If 
their  hearts  are  sound  no  permanent  injury  may  ensue,  unless,  of 
course,  the  strain  be  too  oft  repeated.  In  many  cases  the  children 
have  suffered  from  undetected  rheumatism  and  latent  pericarditis 
or  endocarditis,  and  in  such,  unrestrained  indulgence  will  surely 
result  disastrously  through  the  dcvcloinnent  of  dilatation  of  the 
heart  with  possible  coincident  inflammation  of  some  of  its  struc- 
tures. 

The  heart  of  a  growing  boy  endures  a  degree  of  strain  disas- 
trous in  a  man  of  forty,  and  yet  if  overstrain  be  too  frequently 
repeated  during  one  of  the  "  fatigue  periods  "  of  childhood,  it 
may,  I  am  convinced,  ultimately  enfeeble  the  heart's  resistance 
even  in  a  boy.  The  overdistention  of  the  heart  is  due  probably  to 
ineffectual  systoles,  which  allow  a  residue  of  blood  to  remain  in 
the  distended  cavities,  while  with  the  continuance  of  muscular 
effort  and  deepened  respirations  blood  is  passed  on  to  the  heart 
more  rajudly  and  in  larger  amounts  than  can  be  expelled. 

Another  factor  that  should  not  be  ignored  in  considering  the 
question  of  cardiac  strain  are  those  unknown  "  fatigue  products  " 
developed  during  severe  exercise  and  to  which  particular  attention 
has  boon  called  by  Clifford  Allbutt. 

Symptoms. — The  symptoms  of  cardiac  dilatation  develop 
slowly  or  rapidly  according  to  the  development  of  the  dilatation. 
The  stretching  and  often  thinning  <»f  the  heart-walls  impair  their 
contractility,  and  there  is  a  tendency  to  stasis  within  the  organ 
which  leads  to  loss  of  equilibrium  between  the  arterial  and  venous 
streams.     As  the  heart-power  begins  to  fail  the  pulse  grows  more 


DILATATION  OF   THE   HEART  581 

rapid,  often  irregular  in  force  and  volume,  and  in  many  cases  in- 
termittent. Cardiac  impulse  becomes  weaker,  its  area  of  dulness 
increased,  and  its  sounds  feeble. 

The  patient  begins  to  notice  more  or  less  breatlilessness  on 
exertion  and  a  feeling  of  unwonted  lassitude  that  may  amount 
to  actual  weakness.  Ilis  colour  changes  from  the  reddish  hue  of 
health  to  the  bluish  gray  tint  of  increasing  capillary  stasis.  As 
cardiac  inadequacy  advances,  symptoms  of  visceral  congestion  ap- 
pear. The  urine  lessens  in  amount  and  becomes  of  high  specific 
gravity,  often  containing  a  trace  of  albumin.  The  liver  increases 
in  size,  which  may  cause  a  feeling  of  fulness  in  the  right  hypo- 
chondrium  or  of  dull  pain  in  the  back  below  the  shoulder.  Its 
inferior  margin  becomes  more  or  less  distinctly  palpable,  being 
smooth,  firm,  and  rounded,  and  palpation  of  the  organ  may  be 
somewhat  painful. 

Congestion  within  the  gastro-intestinal  veins  is  shown  by  im- 
pairment of  appetite  and  more  or  less  flatulent  indigestion,  so  that 
the  patient  feels  bloated  after  meals  and  complains  of  windy  con- 
stipated bowel  movement.  Piles  may  develop,  sexual  power  be- 
come deficient,  and  women  are  apt  to  suffer  from  leucorrh(pa  and 
derangement  of  menstrual  function.  Congestion  within  the  lower 
extremities  leads  at  first  to  puffiness  of  the  ankles,  which  by  night 
feel  tense  and  uncomfortable.  When  the  shoes  are  removed  the 
skin  is  found  creased,  and  a  ridge  indicates  where  the  upper  edge 
of  the  shoe  pressed.  After  a  night's  rest  this  swelling  of  the  feet 
and  ankles  may  have  subsided,  but  as  cardiac  incompetence  pro- 
gresses, oedema  remains  permanent.  Pitting  on  pressure  is  now 
pronounced  and  found  to  gradually  extend  upward. 

Thus  gradually  but  steadily  grow  the  symptoms  of  failing  cir- 
culation, and  at  length,  if  the  condition  is  not  arrested  by  treat- 
ment, the  patient  is  compelled  to  keep  his  room.  Pulmonary  con- 
gestion is  no  longer  shown  merely  by  dyspnoea  on  effort,  but  by 
cough  with  frothy,  perhaps  bloody  expectoration,  and  by  orthop- 
noea.  .  Talking  causes  breatlilessness  and  so  much  fatigue  that  the 
patient  dreads  or  even  shuns  the  effort.  Examination  of  the  lungs 
discloses  more  or  less  dulness  at  the  bases  behind  with  fine  crack- 
ling rales — in  short,  the  signs  of  hypostatic  congestion. 

The  apex-beat  is  now  imperceptible  or  is  but  a  feeble  tap 
much  outside  the  left  nipple.     Absolute  and  relative  cardiac  dul- 


582  DISEASES  OF   THE   HEART 

iiess  are  greatly  increased,  of  a  quadrangular  outline,  and  in  ex- 
treme cases  may  extend  from  close  to  the  right  nipple  on  the  one 
hand  nearly  to  the  anterior  axillary  line  on  tlic  other. 

The  heart-sounds  are  almost  inaudihle  and  there  is  very  apt 
to  be  a  systolic  murmur  denoting  relative  mitral  or  tricuspid  in- 
sufficiency or  both.  The  leak  through  the  tricuspid  valves  is 
shown  by  the  positive  venous  pulse  in  the  external  jugulars  and 
liver.  The  veins  of  the  neck  stand  out  like  blue  cords,  and  if  pul- 
sation in  them  is  not  apparent  at  all  times,  becomes  plainly  visible 
so  soon  as  the  patient  coughs  or  makes  a  forcible  expiratory  effort. 
The  pulse  is  now  rapid,  feeble,  and  often  arrhythmic. 

The  state  of  things  has  now  become  pitiable,  and  if  not  re- 
lieved grows  steadily  worse,  with  the  development  of  general 
dropsy,  transudation  into  the  serous  cavities,  somnolence,  even 
low  muttering  delirium  and  death.  This  last  may  occupy  hours, 
appearing  to  come  from  gradual  exhaustion,  or  it  may  be  ushered 
in  by  pulmonary  oedema.  In  such  a  case  fine  crackling  rales  de- 
velop, spread  throughout  the  lungs,  and  at  last  become  plainly 
heard  at  a  distance  with  every  laboured  ros]>iration.  In  other  in- 
stances pulmonary  infarction  occurs,  as  shown  by  cough  and  the 
expectoration  of  bright-red  blood.  In  some  the  heart  stops  ab- 
ruptly and  unexpectedly,  while  the  patient  is  at  rest  or  making 
some  slight  exertion,  although  this  sudden  cessation  of  the  heart's 
action  has  been  preceded  for  several  days  by  signs  of  such  increas- 
ing weakness  that  its  final  arrest  is  scarcely  a  matter  for  surprise. 

In  some  cases  symptoms  of  cardiac  dilatation,  even  extreme, 
persist  for  many  months  or  even  two  or  three  years.  I  recall  a 
man  of  fifty  odd  whom  I  treated  in  1893  and  who  was  a  striking 
example  of  this  chronicity.  For  more  than  a  year  he  had  been 
incapacitated  for  attention  to  business  and  yet  had  managed  to 
keep  about  in  spite  of  very  apparent  shortness  of  breath,  a  rapid, 
exceedingly  arrhythmic  pulse,  enormously  increased  cardiac  dul- 
ness,  and  feeble  heart-sounds.  The  liver  could  be  felt  thin-bor- 
dered and  hard,  and  this  patient  eventually  died  apparently  from 
the  pressure-eifects  of  ascites  rather  than  from  independent  asys- 
tolism.  This  man's  heart  was  undoubtedly  degenerated  and  very 
thin-walled.  It  might  be  reckoned  as  an  example  of  cardiac  in- 
a(l('(|uacy  from  chronic  myocarditis,  but  it  was  a  typical  picture 
of  chrcjiiic  dilatation  of  the  heart. 


DILATATION  OF  THE  HEART  583 

I  have  recently  treated  with  liiglily  gratifying  results,  by 
means  of  batlis  and  resistance  exercises,  ii  powerfully  built  man 
of  thirty-eight  who  was  suffering  from  the  effects  of  heart-strain 
four  years  before.  When  in  apparently  perfect  health  he  endured 
a  day  of  terrible  fatigue  from  the  exertion  of  journeying  in  a 
severe  snow-storm  at  the  altitude  of  18,000  feet.  By  night  he  was 
completely  exhausted,  looked  blue,  felt  cold,  had  a  feeling  of  great 
prtrcordial  oppression,  and  could  not  get  his  breath.  After  a  few 
days'  rest  he  felt  better  and  returned  to  the  East.  He  remained 
at  business,  but  when  summer  came  on,  Avent  abroad  for  a  rest, 
and  in  London  consulted  a  well-known  medical  authority.  By 
him  he  was  told  he  had  suffered  a  heart-strain  and  was  advised  to 
give  up  business.  He  did  not  do  so,  however,  with  the  result 
that  he  gradually  developed  symptoms  of  chronic  heart-disease. 
For  some  months  before  I  saw  him  he  suffered  from  dyspnoea  of 
effort,  a  feeling  by  night  of  profound  exhaustion,  and  the  convic- 
tion that  he  was  liable  to  die  suddenly  at  any  time.  He  neverthe- 
less remained  at  business. 

When  I  first  saw^  him  he  presented  the  signs  of  mitral  regurgi- 
tation with  secondary  enlargement  of  the  heart,  chiefly  of  the  left 
ventricle.  Lungs  were  negative,  but  the  liver  was  palpable. 
There  was  no  pitting,  but  the  tissues  everywhere  felt  tense  and 
hard,  and  the  patient  said  he  "  felt  swollen."  Preliminary  treat- 
ment by  rest  in  bed,  cathartics,  and  a  milk  diet  for  two  days  re- 
duced capillary  stasis,  improved  the  quality  of  the  pulse,  and  re- 
moved the  patient's  sense  of  air-hunger.  There  was  2  per  cent  of 
albumin  in  the  urine,  but  although  repeated  search  was  made  for 
casts,  they  were  never  found. 

At  the  end  of  less  than  four  months  this  patient  declared  he 
felt  perfectly  well  and  desired  to  return  to  business.  The  heart 
w^as  manifestly  smaller  and  its  action  greatly  improved,  but  the 
mitral  systolic  murmur  still  remained.  It  was  less  loud  and  less 
harsh,  however,  and  the  first  sound,  originally  inaudible,  could 
be  heard  distinctly.  The  liver  could  not  be  felt,  but  albuminuria 
persisted.  This  man  had  never  had  articular  rheumatism  or  any 
disease  to  lead  to  endocarditis,  and  prior  to  his  arduous  mountain 
climbing  had  never  had  even  the  slightest  symptoms  of  heart 
weakness.  I  have  no  doubt  that  his  heart-muscle  has  suffered  in 
its  integrity,  but  I  look  upon  this  as  an  instance  of  chronic  left- 


584  DISEASES  OF  THE   HEART 

ventricle  dilatation  due  primarily  to  strain  and  leading  to  relative 
mitral  incompetence. 

Acute  dilatation  of  tlie  heart  from  strain  most  commonly 
affects  the  right  ventricle,  but  it  may  also  take  place  in  the  left. 
This  was  shown  in  the  cases  of  the  young  men  who  were  examined 
by  Harold  Williams  immediately  before  and  after  a  run  of  twenty- 
five  miles.  Cardiac  dilatation  was  shown  by  exhaustion,  cyanosis, 
a  rapid  thready  pulse,  manifest  increase  in  heart's  dulness  both 
to  right  and  left,  and  by  a  systolic  murmur  having  the  characters 
of  a  mitral  bruit.  The  safety-valve  action  of  tricuspid  regurgita- 
tion may  be  rather  quickly  induced  as  compared  to  the  time  it 
would  take  to  set  up  such  a  left-ventricle  dilatation  as  would  pro- 
duce relative  mitral  incompetence.  In  a  run  of  twenty-five  miles 
requiring  three  or  four  hours,  time  would  be  given  for  the  safety- 
valve  action  of  mitral  insufficiency  to  occur.  Were  this  not  so,  the 
left  ventricle  would  be  subjected  to  a  degree  of  strain  that  might 
prove  dangerous  and  even  fatal. 

The  symptoms  of  acute  heart-strain  are  those  of  deficient  arte- 
rial circulation  (relative  arterial  auu'mia),  a  rapid,  weak,  and  it 
may  be  irregular  or  intermittent  pulse  with  signs  of  an  overloaded 
venous  and  pulmonary  system,  dyspnoea,  exhaustion,  pra^cordial 
discomfort,  perhaps  pain,  and  cyanosis,  congestion  of  the  liver,  and 
positive  venous  pulse  of  tricuspid  regurgitation. 

Within  the  last  year  I  have  seen  two  instances  of  acutely  in- 
duced dilatation  of  the  right  ventricle  in  powerfully  built  young 
men  belonging  to  college  foot-ball  teams.  One  of  them  walked  off 
the  field  after  the  contest  was  over,  but  he  looked  blue  in  the  face, 
complained  of  dull  pain  behind  the  lower  end  of  the  sternum,  and 
the  physician  having  charge  of  the  team  detected  increase  of  abso- 
lute dulness  to  the  right.  Symptoms  did  not  disappear  for  a  num- 
ber of  days,  and  it  was  months  before  the  heart's  action  regained 
its  wonted  steadiness. 

When  the  heart-muscle  is  healthy,  acute  dilatation  from  over- 
strain may  be  recovered  from,  yet  if  too  frequently  repeated  may 
without  doubt  result  in  permanent  cardiac  incompetence.  I  be- 
lieve this  is  a  very  positive  danger  attending  college  athletics,  par- 
ticularly in  foot-ball  and  rowing  matches. 

When  the  heart-muscle  is  not  healthy,  and  therefore  when  per- 
sons have  passed  their  forty-fifth  year  and  have  arrived  at  a  time 


DILATATIOfN  OF  THE   HEART  585 

of  life  in  which  the  state  of  the  myocardiinn  is  questionable,  acute 
cardiac  dilatation  from  overstrain  becomes  a  very  serious  matter. 
The  first  symptoms  of  heart-strain  may  be  recovered  from,  but 
more  or  less  inadequacy  is  likely  to  remain.  In  time,  as  a  result 
of  renewed  but  less  severe  strain,  evidence  of  weakness  sets  in 
and  the  patient  ultimately  presents  a  clinical  picture  of  gradually 
increasing  dilatation  of  the  heart. 

Physical  Signs. — Inspection. — The  multiplicity  of  condi- 
tions which  affect  the  results  of  inspection  renders  this  means  of 
investigation  of  comparatively  small  value.  The  eye  may  per- 
ceive the  well-known  manifestations  of  cardiac  weakness,  but  it 
cannot  furnish  information  as  to  the  actual  state  of  the  heart. 
There  is  usually  an  absence  of  visible  cardiac  impulse,  but  this 
alone  is  of  no  value,  since  it  is  normal  to  many  individuals  to 
have  no  visible  apex-beat  on  account  of  the  volume  of  the  lungs 
or  the  thickness  of  the  chest-wall.  In  emphysema,  which  so  com- 
monly leads  to  ultimate  dilatation  of  the  right  heart,  visible  im- 
pulse is  also  likely  to  be  wanting.  In  all  cases  in  which  the  apex- 
beat  is  not  plainly  visible  the  patient  should  be  placed  in  a  strong 
light  and  inspection  made  across  the  front  of  the  chest  from  the 
side  or  from  above  downward.  If  dilatation  exists  a  feeble  aj)ex- 
shock  may  thus  be  sometimes  perceived  outside  of  and  below  the 
nipple  or  in  the  epigastric  notch. 

Palpation. — Aside  from  the  knowledge  which  this  affords  con- 
cerning the  pulse  and  hepatic  congestion,  palpation  is  of  service  in 
the  estimation  of  the  feebleness  or  strength  of  cardiac  contractions. 
Thin-walled  and  dilated  hearts  may  give  no  perceptible  shock  to 
the  chest-wall,  or  they  may  occasionally  produce  a  sudden  quick 
tap  whenever  the  organ  gathers  itself,  as  it  were,  for  an  extra 
effort.  When  the  apex-beat  persists,  it  is  not  like  the  broad  heav- 
ing impulse  of  hypertrophy,  but  is  a  circumscribed  feeble  stroke 
of  a  slapping  character.  This  is  particularly  the  case  in  long- 
standing dilatation  with  still  some  degree  of  efficiency. 

Percussion. — This  is,  as  a  rule,  our  most  valuable  means  of 
determining  if  dilatation  of  the  heart  is  present,  but  it  may  afford 
very  unreliable  evidence  in  cases  of  pulmonary  emphysema.  If 
the  state  of  the  lungs  and  of  the  thoracic  parietes  renders  percus- 
sion available  and  if  dilatation  exists,  the  area  of  deep-seated  if 
not  of  superficial  dulness  is  found  increased  in  accordance  with  the 


586  DISEASES  OF  THE   HEART 

degree  of  dilatation  and  the  chambers  affected.  In  dilatation  of 
the  left  ventricle  relative  dulness  is  increased  towards  the  left  and 
upward,  while  in  stretching  of  the  right  heart  it  is  augmented  to 
the  right  and  downward.  When  general  dilatation  of  the  heart 
exists  the  area  of  dulness  is  found  to  have  assumed  a  quadrangular 
outline  with  broadly  rounded  corners  and  sides. 

Auscultation. — The  licf|rt-sounds  are  feeble,  altered  in  intensity 
and  rhythm,  and  are  frequently  accompanied  or  obscured  by  nuir- 
murs  of  relative  or  muscular  mitral  or  tricuspid  incompetence.  The 
systolic  tone  becomes  shortened  and  valvular  like  the  second,  and 
with  lessening  of  the  long  pause  the  rhythm  of  the  sounds  tends  to 
assume  that  of  the  ticking  of  a  small  clock  or  watch.  In  cases  of 
gi'eat  weakness  and  rapidity  of  heart-action  the  tones  follow  each 
other  in  quick  succession,  or  but  a  single  sound  may  be  detected. 
The  aortic  second  tone  is  usually  diminished,  while  the  pulmonic 
second  is  accentuated.  If  murmurs  exist,  they  are,  as  already  stated, 
those  of  relative  or  muscular  incompetence  of  one  or  both  auriculo- 
ventricular  valves  depending  on  the  degree  of  dilatiition.  The 
auscultator  should  not  forget,  however,  that  it  is  possible  for  bruits 
of  pre-existing  valvular  disease  to  be  present,  and  therefore  he 
must  not  hastily  conclude  that  the  murmur  is  necessarily  due  to 
dilatation  alone.  In  many  cases  he  must  await  the  result  of  treat- 
ment before  deciding  definitely  on  its  real  nature. 

Diagnosis. — The  recognition  of  cardiac  dilatation  is  ordi- 
narily nut  difficult,  especially  if  it  has  been  acutely  induced  or  has 
progressed  to  the  production  of  considerable  inadequacy.  Minor 
degrees  of  stretching  are  not  always  easy  of  detection  and  require 
minute  inquiiy  into  the  history  and  symptoms,  as  well  as  pains- 
taking physical  examination.  In  slowly  induced  dilatation  there 
is  history  of  gradual  onset  and  progressive  increase  of  symptoms 
of  cardiac  incompetence,  while  tliere  are  clinical  findings  of  (1)  a 
more  or  less  rapid  and  feeble,  it  may  be  irregular  or  intermittent, 
pulse;  (2)  feeble,  tapping,  or  even  imperceptible  cardiac  impulse; 
(3)  increase  of  relative  and  perhaps  superficial  dulness  in  one  or 
nion;  directions  according  to  the  cliandx'r  affected;  (4)  feeble  tick- 
ing sounds  and  perhaps  systolic  munnui's  of  relative  or  muscular 
mitral  or  tricuspid  insufficiency. 

In  acute  overstrain  the  phenomena  of  cardiac  embarrassment 
follow  some  unusual  exertion  and  are  easily  recognised,  while  the 


DILATATION  OF  THE  HEART  587 

patient  is  apt  to  display  more  or  less  cyanosis  and  other  evidence 
of  impending  stasis. 

Differential  Diagnosis. — Acute  dilatation  of  the  heart  can 
scarcely  be  mistaken  or  confounded  with  any  other  condition  pro- 
vided due  attention  is  paid  to  history  and  objective  symptoms. 
Distention  of  the  cardiac  cavities  that  has  developed  more  slowly 
and  has  grown  extreme  may,  however,  be  mistaken  for  pericar- 
dial effusion.  The  differential  points  are  fully  dealt  with  in  that 
chapter,  but  special  emphasis  may  here  be  laid  on  the  necessity 
of  determining  the  relation  of  the  outer  and  inferior  margin 
of  deep-seated  dulness  to  the  position  of  the  apex-beat.  In  car- 
diac dilatation  dulness  does  not  pass  beyond  the  limits  of  car- 
diac impulse,  whereas  in  pericardial  distention  the  apex-im- 
pulse is  situated  within  the  outer  border  of  dulness.  This, 
and  this  alone,  is  the  trustworthy  criterion  of  difference  between 
the  two  affections.  In  other  respects  there  is  often  a  striking 
similarity. 

Dilatation  and  hypertrophy  can  scarcely  be  confounded  if  due 
attention  is  paid  to  the  characters  of  the  pulse,  to  the  nature  of 
the  impulse,  and  to  the  greater  feebleness  and  rapidity  of  the 
sounds  in  dilatation.  A  simply  dilated  and  yet  not  specially  de- 
generated heart  cannot  often  be  distinguished  from  a  degenerated 
and  hence  secondarily  dilated  organ,  and  it  is  not  always  prudent 
to  attempt  such  distinction. 

Prognosis. — Dilatation  of  the  heart  should  never  be  regarded 
as  a  trivial  matter,  and  yet  the  degree  of  its  gravity  depends  upon 
the  state  of  the  heart-muscle,  the  extent  of  the  dilatation,  and  the 
length  of  time  it  has  existed.  It  is  the  integrity  of  the  myocar- 
dium in  the  young  and  in  trained  athletes  which  in  them  makes 
the  heart  recover  so  quickly  and  well  from  the  overdistention 
caused  by  strain.  On  the  other  hand,  it  is  the  likelihood  of  the 
heart-walls  being  not  quite  sound  which  renders  prognosis  serious 
when  dilatation  supplants  hypertrophy  or  when  elderly  individ- 
uals suffer  heart-strain.  Stiffened  arteries  do  not  necessarily 
mean  that  the  heart-walls  are  seriously  degenerated,  and  experi- 
ence abundantly  proves  that  in  some  cases  proper  treatment  may 
restore  a  dilated  heart  even  when  the  vascular  coats  are  thickened. 
ISTevertheless,  under  such  conditions  stretching  of  the  cardiac 
chambers  is  always  a  grave  affair,  and  only  too  often  there  is  but 


588  DISEASES  OF   THE   HEART 

little  prospect  of  the  heart-walls  again  becoming  as  sound  as  before 
the  injury. 

Cardiac  dilatation  associated  with  a  granular  kidney  may  al- 
ways be  said  to  furnish  a  very  grave  prognosis,  for  the  resistance 
in  the  arterial  system  is  so  great  that  in  all  likelihood  the  heart 
has  been  gradually  yielding,  and  having  once  given  way,  cannot  re- 
gain its  lost  adequacy.  In  such  a  case  the  prognosis  depends  both 
upon  the  state  of  the  heart-muscle  and  the  possibility  of  lessening 
the  high  pulse-tension  by  treatment. 

In  the  face  of  both  arteriosclerosis  and  interstitial  nephritis 
a  seriously  dilated  heart  is  likely  never  again  to  recover  its  former 
compensatory  hypertrophy^ 

It  is  so  evident  a  fact  as  to  scarcely  require  statement  that 
the  more  extensive  the  dilatation  the  more  serious  the  prognosis. 
With  care  and  proper  management  minor  degrees  of  the  condition 
may  endure  for  a  long  time — even  years — yet  in  such  a  case  the 
tenure  of  life  is  always  uncertain,  for  the  reason  that  some  addi- 
tional and  unexpected  strain  may  at  any  time  convert  a  not  alto- 
gether unfavourable  into  a  most  serious  prognosis. 

Stretching  of  the  auricles  or  of  the  right  ventricle  is  not  so 
grave  a  matter  as  is  left-ventricle  dilatation.  Owing  to  the  thin- 
ness of  their  walls  they  may  not  be  so  amenable  to  treatment — that 
is,  not  so  likely  to  have  their  hypertrophy  restored ;  but  on  the 
other  hand,  the  right  ventricle  is  more  likely  to  be  relieved  by 
stretching  of  its  auriculo-ventricular  ring,  and  therefore  is  less 
liable  to  paralytic  overdistention  and  diastolic  arrest.  This  con- 
sideration leads  me  to  the  belief  that  in  cases  of  left-ventricle  dila- 
tation the  development  of  a  systolic  murmur  at  the  apex  is  a 
favourable  rather  than  an  unfavourable  prognostic  indication. 
Such  a  murmur  is  usually  held  to  indicate  relative  mitral  insuffi- 
ciency, and  by  the  giving  way  of  the  mitral  valve  a  part  of  the 
excessive  endocardial  blood-pressure  becomes  transferred  to  the 
auricle  and  pulmonary  veins,  and  thus  the  wall  of  tlie  left  ventri- 
cle is  relieved,  in  a  measure  at  least.  I  can  recall  more  than  one 
instance  of  sudden  and  unexpected  death  in  men  whose  hearts 
were  seriously  dilated  and  in  whom  such  a  systolic  apex-murmur 
did  not  exist.  On  the  otlicr  IuiihI,  T  liavc  iiioi-c  tlian  once  observed 
that  when  the  mitral  valve  gave  way  tlio  progress  to  asystolism 
was  gradual,  and  death  was  usually  preceded  by  the  symptoms  and 


DILATATION  OF  THE  HEART  589 

signs  of  venous  stasis,  extending  through  a  period  of  weeks  or 
months.  « 

It  is  also  evident  that  prognosis  is  largely  governed  by  the 
length  of  time  the  dilatation  has  existed.  If  the  myocardium  is 
still  healthy,  as  in  the  young,  a  chronic  dilatation  may  yet  be 
recovered  from.  In  persons  past  middle  age  the  condition  is 
likely  to  resist  treatment  if  it  has  become  chronic,  and  if  in  such 
the  pulse  is  persistently  arrhythmic,  it  is  to  be  looked  upon  as  an  in- 
dication that  the  heart-muscle  is  not  sound  or  that  the  auricles  are 
greatly  dilated.  According  to  Radizewsky,  habitual  irregularity 
of  the  pulse  points  to  preponderating  degeneration  of  the  walls  of 
one  or  both  auricles.  If  this  be  correct,  then  arrhythmia  in  con- 
nection with  chronic  dilatation  of  the  heart  is  a  better  prognostic 
sign  as  regards  length  of  life  than  is  tachycardia  with  perfect 
regularity  of  rhythm  due  to  a  dilated  ventricle.  In  acute  dilatation 
from  overstrain,  as  in  foot-ball  or  mountain  climbing,  the  progno- 
sis is  as  a  rule  good,  for  with  rest  and  proper  treatment  the  heart 
is  likely  to  return  to  its  former  healthy  condition.  Repetitions  of 
its  abuse  may,  however,  eventually  induce  j^ermanent  inadequacy. 

Another  element  that  enters  into  the  question  of  prognosis  is 
the  degree  of  subjective  symptoms  produced  by  the  dilatation. 
If  dyspnoea  be  less  than  one  would  be  led  to  expect  from  the  appar- 
ent gravity  of  the  condition,  the  case  is  likely  to  pursue  a  chronic 
course ;  if,  on  the  other  hand,  the  shortness  of  breath  be  out  of 
proportion  to  the  apparent  size  of  the  organ,  or  to  the  amount  of 
exertion  performed  by  the  patient,  or  if  the  dyspnoea  assumes  the 
form  of  cardiac  asthma,  then  the  prognosis  is  bad,  unless  the 
urgency  of  this  symptom  can  be  accounted  for  by  an  associated 
emphysema  or  bronchitis. 

If  skilful  treatment  succeeds  in  producing  only  temporary  im- 
provement, and  the  heart  drops  back  to  its  former  state  so  soon 
as  treatment  is  discontinued,  or  less  vigorous,  it  is  an  indication 
that  the  heart-muscle  is  either  too  weak  to  be  regenerated,  or  the 
peripheral  resistance  is  too  great  to  be  permanently  overcome.  A 
steady  though  gradual  loss  of  ground,  in  spite  of  treatment,  proves 
that  very  little  is  to  be  expected  from  any  management,  no  matter 
how  skilful. 

Except  ill  cardiac  strain  of  effort  in  the  young,  one  should 
never  venture  to  prognosticate  the  length  of  time  it  will  take  for 


590  DISEASES  OF  THE   HEART 

the  heart  to  be  restored  to  health,  or  in  those  in  which  this  is  mani- 
festly impossible,  to  predict  how  long  the  disease  is  likely  to  last. 
If  the  left  heart  is  the  one  chiefly  affected,  the  end  may  come  sud- 
denly and  unexpectedly,  but  in  those  cases  in  which  the  right  heart 
is  the  one  chiefly  at  fault,  and  particularly  when  the  right  auricle 
is  much  dilated,  pulmonary  infarcts  are  very  likely  to  occur  and 
to  be  the  immediately  determining  cause  of  death. 

Two  states  of  mind  on  the  part  of  the  patient,  if  they  come  on 
after  the  disease  has  existed  for  some  time,  and  serious  symptoms 
of  stasis  are  present,  always  make  me  apprehensive  of  the  near 
approach  of  the  end.  These  are,  great  restlessness  and  an  ill- 
defined  nervousness  that  keep  the  patient  constantly  moving 
about,  and  on  the  other  hand  a  sudden  lull  in  the  patient's  sense 
of  distress.  After  days  or  perhaps  weeks  of  severe  suffering  he 
suddenly  has  a  day  in  which  he  feels  remarkably  well  and  free 
from  distress.  This  is  often  like  the  calm  that  precedes  the  storm. 
I  have  more  than  once  seen  death  speedily  succeed  such  a  day  of 
apparent  well-being.  Apropos  of  the  former  state  I  recall  a  large 
middle-aged  num  presenting  all  the  symptoms  and  signs  of  ex- 
treme cardiac  dilatation  whom  I  examined  in  consultation  with 
Dr.  Harrison  late  one  afternoon  and  in  whom  I  saw  no  evidence 
that  the  end  was  imminent;  he  had  been  in  that  condition  for  a 
week,  and,  although  very  dyspnceic,  walked  into  an  adjoining 
room.  He  displayed,  however,  an  indescribable  restlessness,  and 
less  tliaii  tlirec  hours  after  we  left  him  he  died  suddenly. 

Treatment. — In  dilatation  of  the  heart  suddenly  induced 
through  strain  the  first  indication  is  to  place  the  patient  at  rest 
in  the  recumbent  or  semi-recumbent  position  for  the  purpose  of 
lessening  the  heart's  work  so  far  as  that  is  possible.  Muscular  in- 
action and  a  more  tranquil  respiration  bring  the  venous  blood  to 
the  right  heart  less  rapidly,  and  if  the  circulatory  apparatus  is 
healthy,  as  in  the  youthful  athlete,  iSTaturc  alone,  under  favourable 
conditions,  will  speedily  effect  a  restoration  of  the  blood-stream  to 
its  former  equilibrium. 

If,  on  the  contrary,  the  patient's  age  or  state  of  general  nutri- 
tion justifies  the  inference  that  the  heart  cannot  return  to  normal 
without  further  aid,  tlicii  a  morcui-ial  ])ill  and  digitalis  should  be 
prescribed.  15y  uiiloadiui:  I  lie  portal  system  the  cathartic  tends 
to  restore  balance  within  the  abdominal  vessels  and  secondarily 


DILATATION  OP  THE  HEART  591 

in  the  system  at  large.  Five  grains  of  bine  mass  followed  by  ^^ 
onnce  of  Epsom  salts  eight  honrs  thereafter,  or  a  grain  or  two  of 
calomel  at  bedtime  and  a  glassful  of  the  solution  of  citrate  of 
magnesia  next  morning,  or  any  one  of  the  numerous  aperient 
waters  in  the  market,  will  prove  highly  efficient  to  that  end. 

The  purjiose  of  the  digitalis  is  to  slow  down  the  heart  and  en- 
able it  to  empty  its  distended  cavities  effectively.  This  may  be 
accomplished  by  the  administration  of  10  to  15  minims  of  the 
tincture  every  six  hours  for  four  or  five  days.  Improvement  will 
be  shown  by  a  reduction  in  the  rate  and  corresponding  gain  in  the 
force  and  strength  of  the  pulse,  by  disappearance  of  cyanosis  and 
other  signs  of  venous  congestion,  by  increased  diuresis,  and  a 
gradual  return  to  normal  in  the  size  and  sounds  of  the  heart. 
Strychnine  and  nitroglycerin  will  probably  not  be  required.  It 
is  well,  however,  to  insist  on  light  yet  nutritious  diet  until  the 
normal  state  of  the  circulation  has  been  regained. 

When  permanent  cardiac  insufficiency  is  threatened  from  re- 
peated heart-strain  or  from  the  gradual  giving  way  of  hypertrophy 
in  the  face  of  relatively  too  great  peripheral  resistance,  the  prin- 
ciples of  treatnient  must  be  the  same  as  in  any  other  form  of 
heart-weakness.  The  first  indication  is  to  relieve  the  overtaxed 
heart.  Therefore  the  patient  must  be  put  at  physical  rest  for  a 
length  of  time  which  is  to  be  determined  by  results.  'To  the  pa- 
tient's query,  "  How  long  must  I  stay  in  bed  ?  "  do  not  permit 
yourself  to  make  a  definite  answer,  but  tell  him  that  is  to  be  de- 
termined by  the  rapidity  and  degree  of  improvement.  In  other 
respects  the  same  general  plan  of  action  previously  detailed  for 
cases  of  lost  compensation  is  to  be  followed,  but  varied  to  meet 
the  peculiarities  of  each  case. 

Most  cases  of  cardiac  dilatation  which  the  physician  is  called 
on  to  treat  are  not  instances  of  acute  strain,  but  of  chronic  cardiac 
insufficiency.  They  are  to  be  managed,  therefore,  in  accordance 
with  the  principles  laid  down  for  the  treatment  of  inadequacy 
from  chronic  myocarditis,  and  the  reader  is  referred  to  that  chap- 
ter for  details. 

There  are  three  measures,  however,  of  which  it  may  be  well 
to  speak  with  special  relation  to  cardiac  dilatation : 

(1)  Bloodletting. — Occasionally  a  patient  is  encountered  who 
from  one  cause  or  another  is  suffering  from  great  overdistention  of 


592  DISEASES  OF  THE   HEART 

the  right  heart.  The  action  is  extremely  feeble  and  disordered, 
the  face  is  congested,  the  veins  are  turgid,  dyspnoea  is  profound, 
the  lungs  are  filled  with  rales  of  pulmonary  redema,  there  is  cough 
and  bloody,  frothy  expectoration,  there  is  no  redema,  but  the  ex- 
tremities are  cold  and  cyanosed.  Percussion  shows  enormous 
dilatation  of  the  heart,  and,  so  well  as  can  be  determined,  the 
heart-tones  are  very  weak  and  impure.  Dissolution  appears  immi- 
nent. Under  such  circumstances  the  physician  realizes  that  what- 
ever is  to  bring  relief  must  be  done  quickly. 

There  is  not  time  for  digitalis  and  cathartics  to  be  tried ;  they 
are  too  slow.  In  such  an  extremity  there  is  nothing  that  usually 
affords  such  prompt  relief  as  venesection.  Twenty  or  more  ounces 
of  blood  taken  from  the  arm  are  generally  followed  by  diminution 
of  cyanosis,  noticeable  improvement  in  the  quality  of  the  pulse, 
and  increased  clearness  and  strength  of  the  heart-sounds.  Of 
course  such  improvement  will  be  only  temporary  if  nothing  else 
is  done.  This  treatment  must  be  followed  up,  therefore,  by 
the  judicious  use  of  digitalis,  strychnine,  and  cathartics,  to  secure 
what  is  gained  by  the  abstraction  of  blood,  since  this  latter  is  of 
course  only  a  temporary  measure  resorted  to  foi*  the  dire  emer- 
gency. Many  a  patient's  life  has  been  saved  by  such  treatment, 
but,  unfortunately,  it  will  not  save  all. 

(2)  Nmiheim  Baths. — By  some  authors  who  seem  to  make  a 
fad  of  this  mode  of  treatment  these  saline  and  effervescing  baths 
are  advised  even  in  cases  of  extreme  and  long-standing  dilatation. 
Judging  from  my  experience,  such  treatment  is  a  mistake  in  cases 
in  which,  from  the  arrhythmic  pulse,  enormous  area  of  cardiac 
dulness,  and  feeble  tumultuous  heart-sounds,  it  is  clear  that  the 
cardiac  walls  are  too  thin  to  ever  regain  their  old-time  power.  Th(>- 
oretically  these  baths  should  unload  the  cardiac  cavities  and  tlms 
assist  the  heart  in  its  labours.  As  a  matter  of  fact,  I  believe  in 
these  cases  they  do  not  accomplish  this  result.  Such  persons  can- 
not be  materially  benefited  by  anything,  yet  if  any  remedy  can 
help  them  it  should  be  digitalis,  strychnine,  and  cathartics  judi- 
ciously administered  for  an  indefinite  time. 

(3)  Resistance  Exercises. — If  given  by  an  attendant  who 
thoroughly  understands  how  to  apply  the  proper  degree  of  resist- 
ance to  a  feeble  heart,  these  exercises  may  ])rove  of  real  benefit 
even  to  a  seriously  dilated  heart.     They  ai-e  supposed  to  relieve 


DILATATION  OP   THE   HEART  593 

the  cardiac  cavities  by  diverting  a  part  of  their  contents  to  the 
peripheral  vessels,  and  as  a  matter  of  fact  they  are  followed  by  a 
demonstrable  decrease  in  the  area  of  cardiac  dulness.  Neverthe- 
less I  do  not  believe  it  is  possible  to  create  so  remarkable  a  decrease 
as  is  claimed  by  Theodor  Schott,  who  finds  in  this  effect  a  means 
of  differential  diagnosis  between  a  dilated  organ  and  a  pericardial 
effnsion.  When  employed  in  the  condition  now  considered  they 
must  be  given  with  very  great  gentleness,  and  movements  are  to 
be  omitted  which  necessitate  the  elevation  of  the  arms  above  the 
head  as  well  as  bending  of  the  trunk  at  the  hips,  which  are  capable 
of  augmenting  dyspnosa  and  aggravating  the  dilatation.  Even 
when  permanent  improvement  in  the  patient's  condition  does  not 
result  it  is  generally  found  that  for  a  time  at  least  there  is  a  less- 
ening of  his  distress  and  an  improvement  in  his  colour.  I 
therefore  recommend  their  trial  in  all  cases  of  chronic  cardiac 
dilatation. 

Should  cases  of  chronic  cardiac  incompetence  be  not  improved 
by  the  measures  just  spoken  of,  then  it  is  reasonable  to  infer  that 
the  case  has  passed  beyond  the  stage  in  which  anything  more  is 
to  be  hoped  from  treatment  than  the  amelioration  of  symp- 
toms. One  may  yet  do  what  he  can  with  digitalis,  strychnine, 
nitroglycerin,  diffusible  stimulants,  and  cathartics.  In  the  ma- 
jority of  cases  morphine  will  now  have  to  be  given^  and  if  admin- 
istered hypodermically  to  secure  comfortable  nights,  the  remedy 
is  generally  of  the  greatest  service.  In  many  instances  mor- 
phine thus  given  will  jDrolong  life  and  ease  the  sufferer's  path  to 
the  grave. 

Only  a  few  months  ago  Dr.  George  F.  Roberts,  of  Minneapo- 
lis, called  me  to  see  a  gentleman  of  nearly  sixty  who  presented  a 
typical  picture  of  a  dilated  heart.  The  myocardium  was  probably 
degenerated,  but  his  arteries  were  soft  and  urine  was  negative,  so 
that  one  could  not  say  there  was  more  than  cardiac  incompetence 
from  dilatation.  He  was  in  bed  and  dyspnoeic,  but  his  suffering 
arose  from  vertigo,  which  came  every  few  minutes  and  lasted  from 
a  few  seconds  to  a  minute  or  more.  During  the  vertigo  his  radial 
pulse  wholly  disappeared  and  the  heart-sounds  became  exceedingly 
rapid  and  feeble  but  perfectly  regular ;  the  cavities  were  not  being 
emptied.  Suddenly  the  action  of  the  heart  would  change,  becom- 
ing slow,  strong,  but  irregular ;  the  pulse  would  return  and  the 
39 


594  DISEASES  OP   THE   HEART 

patient  would  exclaim,  "  There !  it  is  gone !  "  meaning,  of  course, 
his  dizziness. 

The  cervical  veins  were  distended,  liver  was  palpable,  urine 
scanty,  but  no  oedema  and  no  turgescence  of  the  superficial  veins 
over  the  trunk  and  limbs.  Cardiac  impulse  was  absent  and  the 
area  of  dulness  enormously  increased  and  of  a  quadrangular  out- 
line. It  seemed  as  if  the  large  vessels  of  the  abdominal  and  portal 
systems  were  holding  the  most  of  the  blood. 

Venesection  was  indicated  and  might  have  afforded  temporary 
relief,  but  for  certain  reasons  it  was  not  performed.  Instead, 
nitroglycerin,  camphor,  and  valerianate  of  caffeine  were  injected 
subcutaneously  at  short  intervals  and  the  bowels  were  opened  by 
calomel  and  a  saline.  Vertigo  was  relieved  by  this  means,  but 
circulation  was  not  materially  improved.  The  heart-walls  were 
too  greatly  stretched  and  probably  degenerated  to  regain  their  ade- 
quacy, and  the  i)atient  died  about  ten  days  subsequently. 

II.    RELATIVE  AND  MUSCULAR  MITRAL  INSUFFICIENCY 

Relative. — By  this  term  is  meant  that  variety  of  incompetence 
which  results  from  over-distention  of  the  left  ventricle  and  is  en- 
countered in  its  most  typical  form  in  the  acute  heart-strain  just 
described.  When  so  produced  the  insufficiency  is  sometimes 
spoken  of  as  primary,  to  distinguish  it  from  the  subdivision  known 
as  secondary.  It  is  the  latter,  or  secondary,  that  not  infrequently 
develops  in  the  late  stage  of  aortic  stenosis  and  regurgitation  and 
has  so  often  been  referred  to  in  the  foregoing  pages. 

Balfour's  terui.  Curable  Mitral  Regurgitation,  was  intended  to 
cover  cases  of  primary  relative  mitral  incompetence,  particularly 
as  seen  in  chlorotic  girls,  since  it  is  very  amenable  to  treatment. 
The  term  was  based  on  the  supposition  of  such  a  stretching  of  the 
mitral  ostium  as  precluded  the  adequate  closure  of  the  valve-flaps. 
In  the  light  of  more  recent  knowledge,  however,  it  is  likely  that 
the  insufficiency  described  by  that  distinguished  author  is  in  reality 
the  form  now  to  be  considered. 

Muscular. — This  term,  which  may  be  applied  to  incompetence 
whether  of  the  mitral  or  tricuspid  valve,  denotes  a  form  of  in- 
sufficiency depending  not  on  over-distention  of  the  ventricle  with 
corresponding  dilatation  of  the  ring,  ])ut  on  a  functional  defect  of 
the  muscular  mechanism  by  which  iioniially  the  valve  is  enabled 


KELATIVE  AND  MUSCULAR  MITRAL  INSUFFICIENCY       595 

to  close.  Tor  our  knowledge  of  the  facts  underlying  this  sub- 
division of  mitral  incompetence  we  are  indebted  to  the  Leipzig 
School,  whose  views  it  must  be  confessed  have  been  very  tardily 
accepted  by  English  and  American  authors. 

Pathology.^ — The  morbid  anatomical  condition  underlying 
relative  insufficiency  of  the  auriculo-ventricular  valves  is  dilatation 
of  the  ventricle.  This  dilatation  must  reach  such  an  extreme  grade, 
however,  as  to  carry  with  it  more  or  less  stretching  of  the  mitral 
ring,  as  shown  by  its  admitting  more  than  three  fingers.  The  valve 
itself  is  structurally  intact,  or  in  cases  of  long  standing  the  cusps 
may  be  longer  and  broader  than  normal  and  the  papillary  muscles 
be  flattened  and  elongated  as  a  result  of  the  pressure  to  which 
they  have  been  subjected.  In  brief,  the  organ  presents  the 
changes  previously  described  under  Dilatation  of  the  Heart,  either 
with  or  without  structural  disease  at  the  aortic  orifice. 

In  muscular  mitral  insufficiency  the  left  ventricle  may  or  may 
not  present  evidence  of  dilatation,  but  if  this  condition  existed  dur- 
ing life  it  was  not  of  so  high  a  grade  as  is  the  case  when  relative 
incompetence  oocurs.  In  many  instances  the  pathologist  is  sur- 
prised by  finding  nothing  at  first  sight  to  explain  the  murmur 
heard  before  death.  The  mitral  ostium  is  not  dilated  and  the 
valves  are  intact. 

Closer  examination,  however,  discloses  changes  in  the  muscula- 
ture which  interfered  with  the  perfect  coaptation  of  the  valve-flaps. 
These  are  the  changes  of  acute  or  chronic  myocarditis,  which 
favour  the  occurrence  of  more  or  less  dilatation  and  defective 
action  on  the  part  of  the  ring  muscle  or  papillaries,  or  both. 

Three  factors  are  concerned  in  the  closure  of  the  auriculo- 
ventricular  valves,  (1)  the  pressure  of  the  blood  within  the  ventri- 
cle upon  their  ventricular  surface,  (2)  the  contraction  of  the  ring 
muscle  at  the  base  of  the  ventricle  by  which  the  orifice  is  nar- 
rowed to  a  mere  chink,  and  (3)  the  contraction  of  the  papillary 
muscles  and  consequent  tightening  of  the  cordse  tendineas.  The 
combined  effect  of  all  these  elements  is  the  perfect  apposition  of 
the  valve-flaps  throughout  practically  their  entire  surface,  and  not 
merely  at  their  margins. 

If  now,  in  consequence  of  inflammation  or  degeneration,  the 
wall  of  the  ventricle  dilates  sufficiently  to  prevent  the  mitral  ostium 
from  becoming  adequately  contracted  during  systole,  or  to  inter- 


596  DISEASES  OP  THE  HEART 

fere  with  the  i^roper  pull  of  the  papillaries,  then  the  condition  is 
present  which  permits  more  or  less  regurgitation;  the  valve  is 
rendered  muscularlj  incompetent.  Consequently,  in  any  case  in 
which  the  clinical  diagnosis  of  mitral  insuthciency  has  been  made 
and  in  which  the  valves  are  found  intact  after  death,  careful 
examination  must  be  made  of  the  state  of  the  myocardium,  since 
in  degeneration  of  the  wall  or  of  the  papillaries  may  be  discovered 
the  pathological   cause  of  the  regurgitation. 

Etiology. — Primary  relative  insufficiency  of  the  mitral  valve 
is  the  result  of  acute  dilatation  of  the  left  ventricle  from  excessive 
physical  exertion,  i.  e.,  acute  strain.  This  was  well  shown  by  Har- 
old Williams's  observations.  He  found  that  of  1-]  healthy  young 
men  examined  immediately  after  a  run  of  25  miles,  11  presented 
appreciable  dilatation  of  the  left  ventricle  with  a  mitral  systolic 
murmur  and  vascular  evidence  of  stasis.  When  the  myocardium 
is  degenerated  and  the  arteries  arc  stiff,  indiscreet  physical  effort 
is  especially  likely  to  occasion  cardiac  overstrain,  and  I  have  more 
than  once  discovered  this  form  of  valvular  incompetence  in  elderly 
men  after  a  business  or  hunting  ti'i])  in  the  Ivocky  Mountains. 

Secondary  relative  mitral  insufficiency  may  be  said  to  be  the 
result  of  chronic  heart-strain.  It  is  jwssible,  therefore,  when  the 
left  ventricle  has  been  compelled  for  a  long  time  to  labour  against 
great  peri])heral  resistance,  as  in  cases  of  acu'tic  stenosis.  It  is  seen 
not  infrequently  in  chronic  interstitial  nephritis  when  the  hyjjer- 
trophied  ventricle  is  no  longer  able  to  cope  with  the  excessive  blood- 
pressure  in  the  aortic  system,  or  when  the  ventricle  struggling  to 
preserve  its  adequacy  is  overpowered  by  the  addition  of  some  un- 
Avonted  ])liysical  or  mental  strain.  Tlie  same  holds  true  of  the  mi- 
tral incoiujK'tence  secondary  to  hmg-standing  aortic  r(\gurgitation. 

The  causes  of  muscular  mitral  itisuffirirnry  are  id(Mitical  with 
those  of  the  secondary  relative  foi-ni.  Less  dilatation  of  the  left 
ventricle  is  required  to  produce  it,  however,  hence  it  is  a  more 
frecpient  occurrence.  ]\roreover,  degeneration  of  tlie  ])apillaries  is 
a  condition  wliicli  often  leads  to  museular  incompetence,  whereas 
it  cannot  pro<luce  the  relative  form.  The  muscular  incoin])etence 
may  likewise  result  from  acute  heart-strain  when  this  is  not  car- 
ried to  the  point  of  extreme  dilatation. 

Acute  myocarditis  is  a  cause  of  tlie  nmscnlai-  form  far  more 
commonly  than  is  recognised.      'Idie  dilatation  may  be  slight  and 


RELATIVE  AND   MUSCULAR  MITRAL  INSUPPICTENCY       597 

escape  recognition,  and  hence  the  apex  murmur  is  generally  sup- 
posed to  indicate  endocarditis.  Such  an  error  is  the  more  likely 
since  the  acute  myocarditis  develops  in  the  course  of  some  acute 
infection,  as  rheumatism,  diphtheria,  typhoid  fever,  etc.  The  ulti- 
mate subsidence  of  the  murmur  jKii-i  passu  with  the  return  of  the 
ventricle  to  normal  size  probably  proves  the  condition  to  have  been 
muscular  and  not  endocarditic. 

The  Curable  Mitral  Regurgitation'  of  chlorosis  and  grave 
ansemia,  which  is  probably  muscular  in  the  strict  sense,  is  due  prob- 
ably to  the  blood-state,  which  by  depriving  the  heart  of  requisite 
nutrition  lessens  its  resisting  power  so  that  a  moderate  grade  of 
dilatation  supervenes. 

Symptoms  are  those  observed  in  cardiac  inadequacy,  and 
need  not  be  detailed  here.  Their  intensity  and,  to  a  certain  extent, 
their  character  depend  upon  the  freedom  of  the  leak  and  the 
rapidity  of  its  development.  In  the  slighter  grades  of  muscular 
mitral  incompetence  symptoms  may  be  so  mild  as  not  to  draw 
attention  to  the  real  seat  of  trouble,  and  it  may  be  difficult  to 
decide  how  much  of  the  clinical  picture  is  due  to  the  leak  and 
how  much  to  the  underlying  cardiac,  vascular,  or  renal  condition. 

Relative  mitral  insufficiency  of  acute  heart-strain  produces 
pronounced  symptoms,  viz.,  prsecordial  distress,  dyspnoea,  a  feel- 
ing of  weakness  that  may  amount  almost  to  syncope,  cyanosis  or  an 
ashen  pallor  of  the  countenance.  Ana?mic  or  chlorotic  girls  with 
"  curable  mitral  regurgitation  "  are  apt  to  display  breathlessness, 
muscular  weakness,  and  sometimes  slight  ankle  puffiness,  which 
is  due  to  the  state  of  the  blood  rather  than  the  heart. 

Physical  signs  are  essentially  the  same  as  in  mitral  regurgi- 
tation of  endocarditic  origin,  but  with  slight  differences.  In  rela- 
tive insufficiency  percussion  is  apt  to  show  greater  increase  of  dul- 
ness  to  the  left,  while  in  muscular  incompetence  the  murmur  is 
more  typically  blowing  and  generally  accompanies,  but  does  not 
replace,  the  first  sound  at  the  apex. 

Diagnosis. — The  recognition  of  the  mitral  insufficiency  is 
generally  easy.  The  difficulty  lies  in  differentiating  the  forms  we 
are  considering  from  the  incompetence  of  endocardial  inflamma- 
tion.    The  main  differential  points  are  the  following: 

(A)  Age,  the  individual  in  most  cases  being  past  forty.  (B) 
History  of  articular  rheumatism  wanting,  but  in  the  primary  rela- 


598  DISEASES  OF  THE  HEART 

live  form  liistory  of  cardiac  strain.  (C)  Habits  and  occupation 
that  tend  to  chronic  myocarditis  and  arteriosclerosis.  (D)  Signs 
of  stiff  arteries  or  interstitial  nephritis  or  both.  (E)  Chlorosis  or 
anaemia  in  females  without  previous  rheumatism.  (F)  The  asso- 
ciation of  an  acute  infection,  as  diphtheria,  typhoid  fever,  influ- 
enza, etc.,  during  which  the  characteristic  murmur  develops. 

The  recognition  of  the  real  nature  of  the  incompetence  is  often 
most  diflicult  if  not  impossible  before  one  has  had  opportunity  to 
observe  the  effect  of  time  and  treatment.  Great  distention  of  the 
left  ventricle  may  enable  one  at  once  to  pronounce  in  favour  of 
a  relative  incompetence,  but  muscular  insufficiency  with  little  or 
no  recognisable  dilatation  may  readily  be  mistaken  for  a  valvulitis. 
An  important  differential  point  is  to  be  found  in  the  characters 
of  the  munnur. 

In  muscular  mitral  incompetence  the  murmur  generally''  accom- 
panies, but  does  not  replace,  the  first  tone  at  the  apex.  It  is  not 
widely  propagated,  being  as  a  rule  circumscribed  to  the  vicinity 
of  the  apex.  It  is  not  so  intense  as  the  mitral  regurgitant  bruit 
of  chronic  endocarditis,  and  may  be  most  plainly  audible  between 
the  left  nipple  and  sternum.  Given  such  a  systolic  murmur  with 
accentuation  of  the  ])ulmonic  second  tone  in  a  person  having  stiff 
vessels,  or  an  impoverishment  of  the  blood  or  one  of  the  acute 
infections  whicli  is  more  likely  to  produce  acute  myocarditis  tlian 
endocarditis,  one  may  with  reasonable  confidence  diagnose  muscu- 
lar mitral  rather  than  relative  or  endocarditic  insufficiency. 

Prognosis. — This  is  determined  by  the  cause,  the  freedom 
of  the  leak  and  the  age  of  the  patient.  The  relative  incompetence 
of  acute  heart-strain  in  the  young  is  likely  to  be  recovered  from 
under  proper  treatment.  The  muscular  incompetence  of  the  mid- 
dle-aged or  senile  may  be  removed  by  suitable  therapy  for  a  time, 
but  is  pretty  sure  to  return.  The  mitral  regurgitation  secondai'v 
to  interstitial  nepliritis  furnishes  a  very  grave  prognosis,  since  the 
iiigh  blood-pressure  precludes  closure  of  the  valve  even  under  the 
most  approved  treatment.  The  mitral  leak  in  the  chlorotic  or 
profoundly  aniemic  is  removable  if  the  blood-state  can  be  corrected, 
and  honco  has  been  termed  "curable." 

Treatment. — This  is  that  of  the  underlying  pathological  con- 
dition to  which,  as  well  as  to  Chapters  XVIT  and  XVIII,  the 
reader  is  referred. 


CHAPTER    XXIII 

FATTY    HEART 

CARDIAC  INADEQUACY  OP  THE  CORPULENT 

Fatty  lieart  is  the  term  most  commonly  employed  to  designate, 
not  fatty  degeneration  of  the  heart-muscle,  but  a  deposit  of  fat  be- 
neath the  epicardium  and  between  the  muscle-fibres — a  condition 
variously  styled  fatty  overgrowth  and  fatty  infiltration. 

Morbid  Anatomy. — In  this  disease  the  subepicardial  layer 
of  adipose  tissue  is  strikingly,  sometimes  enormously,  increased. 
The  fat  is  particularly  abundant  in  the  interventricular  and  inter- 
auricular  grooves,  especially  the  latter,  and  along  the  branches  of 
the  coronary  arteries.  It  is  usually  thicker  over  the  right  than 
over  the  left  ventricle.  It  is  not  only  deposited  on  the  surface 
of  the  organ,  but  makes  its  way  between  the  bundles  of  muscle- 
fibres,  which,  examined  microscopically,  are  seen  to  be  more  or 
less  widely  separated  and  to  have  become  attenuated  or  atrophied. 
In  some  instances  there  may  even  be  masses  of  fat  beneath  the 
endocardium. 

Pathology. — It  is  generally  believed  that  when  cardiac  in- 
sufficiency declares  itself  in  fat  people  it  is  owing  to  an  excessive 
deposit  of  adipose  tissue  upon  the  heart  or  to  fatty  degeneration 
of  the  heart-muscle.  Romberg  has,  however,  set  forth  in  so  ad- 
mirable a  manner  the  real  pathology  of  this  condition  that  I  shall 
avail  myself  of  much  of  what  he  says. 

He  agrees  with  Ley  den  in  the  view  that  the  old  conception  of 
fatty  heart  as  an  independent  affection  must  be  abandoned,  and, 
instead,  makes  the  term  fatty  heart  include  those  disturbances  of 
heart  action  manifested  by  the  obese  which  either  bear  a  direct 
relation  to  their  obesity  or  have  developed  independently^  That 
their  cardiac  insufficiency  is  not  due  to  fatty  overgrowth  is  sub- 
stantiated by  the  observation  that  hearts  loaded  down  with  adipose 

599 


600  DISEASES  OF  THE  HEART 

tissue  have  not  ahvavs  given  signs  of  inadequacy,  and  on  the  other 
hand  that  such  as  were  manifestly  insufficient  during  life  have  not 
always  shown  a  deposit  of  fat  sufficient  to  account  for  the  weak- 
ness. 

The  cause  of  the  heart  difficulty  resides,  therefore,  in  some 
other  condition,  and  this  Eomberg  finds  to  be  relative  smallness 
and  weakness  of  the  heart-muscle — i.  e.,  disproportionate  to  the 
demands  made  upon  it  by  the  condition  of  general  corpulence. 
In  some  fat  but  muscular  individuals  the  heart  is  correspondingly 
large  and  muscular,  and  symptoms  of  cardiac  inadequacy  do  not 
appear.  Other  corpulent  individuals  of  indolent  habits  are  anae- 
mic and  have  a  flabby  musculature.  In  them  the  heart-muscle, 
rendered  weak  and  flabby  through  anaemia  and  want  of  exercise, 
is  incapable  of  responding  adequately  to  the  work  required  of  it, 
by  the  great  exertion  of  moving  the  ponderous  body -mass,  and 
hence  symptoms  of  heart-weakness  appear. 

In  such,  the  heart  is  overtaxed  even  when  the  body  is  in  re- 
pose, and  manifests  its  debility  at  all  times.  In  some  instances  car- 
diac svmptoms  first  make  their  appearance  after  some  unwonted 
exertion  or  after  an  attack  of  influenza  or  some  other  acute  in- 
fectious disease.  In  a  few  cases  disease  of  the  coronary  arteries 
is  responsible  for  an  attack  of  angina  pectoris,  or  for  sudden 
death,  through  rupture  of  the  heart-wall.  But  such  conditions  are 
wholly  independent  of  the  obesity.  This  conception  of  the  fatty 
heart,  entertained  as  it  is  by  two  such  masters  as  Leyden  and 
Romberg,  is  in  strict  accordance  with  daily  observation,  and  makes 
it  clear  why  one  enormously  fat  person  is  capable  of  performing 
a  degree  of  physical  effort  wholly  impossible  to  another  much 
less  obese.  It  is  evident,  also,  how  fallacious  it  may  be  to  diag- 
nose fatty  heart  merely  on  the  ground  of  general  corpulence. 

Etiology. — The  causes  of  an  excessive  growth  of  fat  on  the 
heart  may  be  said  to  be  those  of  obesity  in  general.  There  seems 
to  be  a  marked  tendency  to  corpulence  in  some  families,  and  their 
meml^ers  accumulate  fat  notwithstanding  all  efforts  to  the  con- 
trary. Such  a  predisposition  is  sometimes  witnessed  among  chil- 
dren ;  but  as  a  rule  corpulence  does  not  manifest  itself  until  after 
puberty  or  still  later,  between  the  ages  of  thirty  and  forty.  Age 
itself  is  a  predisposing  factor,  particularly  with  women,  who  show 
a  striking  tendency  to  increased  weight  after  the  menopause. 


FATTY  HEART  601 

The  female  sex  in  general  is  said  to  show  a  greater  inclination 
to  corpulence  than  does  the  male  sex,  yet  the  difference  in  this 
regard  is  probably  to  be  attributed  to  differences  in  occupations 
and  habits,  since  women  generally  take  less  exercise  than  men. 
They  are,  moreover,  apt  to  be  chlorotic  and  ana?mic,  and  it  is  well 
known  that  fat  and  ansemia  often  go  together,  in  consequence 
probably  of  the  diminished  oxidizing  power  of  the  blood.  People 
of  sedentary  pursuits  are  especially  liable  to  take  on  fat,  and  with 
family  inheritance  and  occupation  combined,  obesity  becomes  in- 
evitable. 

Of  all  causes,  the  one  most  potent  next  to  inherited  tendency 
is  consumption  of  food  rich  in  carbohydrates  conjoined  with  an 
excessive  intake  of  fluids.  Gluttony  (luxus  consumption)  con- 
duces to  obesity  even  though  there  is  not  a  relative  disproportion 
in  carbohydrates.  This  is  especially  injurious  when  added  to  in- 
adequate exercise.  The  too  free  drinking  of  fluids  is  another 
potent  factor,  and  when  in  the  form  of  malt  liquors,  fat  may  be 
taken  on  very  rapidly.  The  excessive  use  of  alcohol  in  any  form, 
moreover,  is  said  to  favour  the  development  not  only  of  fat  in 
general,  but  in  particular  of  the  deposit  of  adipose  tissue  upon  the 
heart. 

The  foregoing  are  the  leading  causes  of  fatty  overgrowth,  but 
it  must  be  remembered  that  the  modern  conception  of  fatty  heart 
is  not  necessarily  a  surplus  accumulation  of  adipose  tissue  be- 
neath the  epicardium  and  between  the  bundles  of  muscle-fibres, 
but  a  manifestation  of  cardiac  insufficiency  attributable  primarily 
to  general  obesity.  Consequently,  in  studying  the  etiology  of  the 
heart-weakness  exhibited  by  corpulent  people,  we  must  bear  in 
mind  what  was  said  above  concerning  the  pathology  of  the  fatty 
heart.  Whatever  tends  to  undermine  muscular  strength  in  gen- 
eral produces  a  weak  heart-muscle,  and  in  the  obese  such  influences 
are  specially  deleterious. 

Luxurious  living,  indolent  habits,  excesses  of  all  kinds  (in- 
cluding the  abuse  of  tobacco),  anaemia,  and  chlorosis — all  tend  to 
produce  a  flabby  heart-muscle.  Such  a  heart  is  incapable  of  that 
driving  power  necessary  to  force  the  blood  through  the  extensive 
system  of  capillaries  created  for  the  supply  of  new  adipose  tissue, 
in  addition  to  those  ramifying  in  the  organs,  muscles,,  bones,  etc. 
Under  the  demands  of  a  quiet  existence  such  a  heart  may  show  no 


602  DISEASES  OF  THE  HEART 

incompetence  severe  enough  to  attract  the  person's  attention. 
When,  however, ,  cardiac  inadequacy  makes  its  appearance,  it  is 
gradual  and  insidious,  or  abrupt  in  consequence  of  unwonted 
exertion  or  of  acute  ilhiess.  In  such  cases  the  obesity  is  the  predis- 
posing cause,  and  the  conditions  that  bring  about  heart-strain  the 
exciting  cause. 

Finally,  Romberg  includes  among  the  causes  of  cardiac  insuf- 
ficiency a  too  strenuous  anti-fat  diet  which  is  practically  a  starva- 
tion diet,  and  too  rigorous  depleting  measures  acting  through  the 
skin  and  bowels.  If,  in  addition,  vigorous  exercise  is  taken,  the 
undcrnonrishod  heart-muscle  can  readily  become  overstrained. 

Symptoms. — There  is  nothing  in  the  symptoms  peculiar  to 
the  disease  under  consideration.  Shortness  of  breath  is  usually 
the  first  symptom  to  make  its  appearance,  but  such  persons  are  so 
accustomed  to  quickening  of  respiration  during  exertion  that  they 
give  no  heed  to  it  until  it  has  reached  a  degree  of  considerable  or 
continuous  dyspna'a.  At  first,  embarrassment  of  breathing  is 
only  noticed  during  hurry  or  the  effort  of  ascending  stairs,  but 
subsequently  it  is  called  forth  by  the  mere  act  of  rising  from  a 
chair  and  walking  across  the  room.  Stooping  or  bending  forward 
is  apt  to  cause  great  dyspna^a ;  and  as  cardiac  feebleness  pro- 
gresses, distressing  shortness  of  breath  declares  itself  during  the 
taking  of  food,  and  there  is  panting  respiration  even  during  con- 
versation. At  length  in  this,  as  in  other  forms  of  heart-disease, 
a  stage  of  orthopnoea  is  reached  when  dyspnoea  becomes  habitual, 
even  while  the  patient  is  at  rest. 

Another  early  symptom  in  some  cases  is  lightness  of  the  head 
or  vertigo,  especially  likely  to  apj)ear  when  the  j)aticnt  gets  on  to 
his  feet  or  changes  the  recumbent  for  the  upright  position.  In 
some  instances  there  are  attacks  of  veritable  syncope,  the  feeble 
heart  failing  temporarily  to  maintain  cerebral  circulation.  It 
sometimes  happens  that  a  patient  dies  in  such  a  syncopal  attack 
under  appearances  which  caused  Stokes  to  term  it  "  apoplecti- 
form." 

Another  symptom  also  observed  in  the  early  stage  of  the  dis- 
ease is  acceleration  of  the  ])ulse.  Stokes,  Walshe,  and  other  early 
English  writers  laid  particular  stress  on  slowness  of  the  pulse  as  a 
sign  of  fatty  heart,  but  as  a  mnttor  of  fact  it  is  more  common  for 
the  pulse  to  exhiljit  an  increase  in  frocpiency.     It  is  also  apt  to  be 


FATTY   HEART  603 

small  nnd  fcoblo,  althouoh  associated  arterial  sclerosis  or  chronic 
nephritis  may  give  it  undue  tension.  Another  not  infrequent  fea- 
ture of  the  pulse  is  instability — i.  e.,  a  lack  of  steadiness  in  its 
rhythm — fluctuations  taking  place  in  its  rate  without  apparent 
cause.  Irregularity  in  force  and  volume  and  intermittence,  how- 
ever, are  not  common. 

In  some  instances  the  earliest  symptoms  are  referable  chiefly 
to  the  digestive  organs.  The  patient  finds  that  his  usually  small 
appetite  has  become  still  more  diminished,  or  that  so  soon  as  he 
has  eaten  a  little  he  is  oppressed  by  an  uncomfortable  sense  of 
fulness  and  shortness  of  breath.  Unquenchable  thirst  impels  him 
to  drink  large  amounts  of  water  or  tea,  which  but  increase  his 
oppression,  and  he  is  annoyed  by  frequent  eructations  of  gas.  His 
bowels  are  sluggish  and  constipated,  and  his  urine  becomes  scanty 
and  high-coloured.  He  is  apt  to  fall  asleep  in  the  chair,  particu- 
larly after  meals,  while  at  night  he  is  wakeful,  or  if  he  sleeps, 
is  harassed  by  nightmare  and  dreams.  Headaches,  usually  dull 
and  heavy,  but  sometimes  of  a  neuralgic  character,  are  not  un- 
common. 

If  the  circulation  has  not  become  too  seriously  embarrassed, 
and  particularly  if  the  heart-muscle  is  intact,  the  symptoms  being 
due  to  a  disparity  between  the  size  of  the  body  and  the  power  of 
the  heart,  then  measures  calculated  to  reduce  the  obesity  and  thus 
restore  the  proper  relation  between  body  weight  and  heart  power 
may  reinstate  the  patient's  health.  In  very  many  cases,  unfortu- 
nately, this  is  impossible;  the  heart-muscle  has  become  seriously 
damaged  through  atrophy  or  degeneration  or  coronary  sclerosis, 
or  serious  dilatation  has  been  set  up  in  consequence  of  long  years 
of  overstrain,  or  as  the  result  of  some  single  indiscreet  effort. 
Symptoms  of  failing  circulation  now  appear  and  progress  steadily, 
it  may  be  rapidly.  Cough  and  frothy  mucous  expectoration,  at- 
tacks of  asthma  and  cardiac  pain  of  an  anginoid  character,  or 
even  of  true  angina  pectoris,  are  added  to  the  previously  existing 
dyspnoea.  Hepatic  congestion  and  tenderness,  scanty  albuminous 
urine,  and  oedema  of  the  ankles  are  discovered,  and  before  long 
the  patient  presents  the  well-known  picture  of  the  final  stage  of 
heart-disease  which  has  been  so  often  described  in  these  pages.  It 
scarcely  requires  physical  examination  of  the  chest  to  convince 
one  that  the  heart  is  dilated  and  overburdened,     Orthopnoea  com- 


604  DISEASES   OF   THE   HEART 

pels  the  patient  to  remain  in  bis  easy  chair,  and  in  the  hope  of 
obtaining  still  greater  ease,  or  of  lessening  the  dropsy,  the  swollen, 
tense,  and  shiny  legs  are  supported  upon  another  chair  or  stool. 
Xurses  stand  by  his  side  to  administer  stimulants,  or  by  fanning 
him,  to  mitigate  his  attacks  of  dysf)noea.  Sleep  visits  him  but 
fitfully,  if  at  all,  and  neither  day  nor  night  brings  him  relief  from 
his  torment. 

In  this  manner  one  week  merges  into  another,  and  he  is  to  be 
accounted  fortunate  when  pulmonary  oedema  ends  his  suffering, 
or  the  heart  stops  suddenly  and  imexpectedly.  It  is  the  same  old 
story  over  and  over,  varied  only  by  the  greater  prominence  of 
some  symptoms  in  one  case  and  of  others  in  another,  or  by  the 
longer  or  shorter  duration  of  the  struggle. 

Physical  Signs. — Inspection. — Obesity  renders  examina- 
tion of  the  thoracic  and  abdominal  organs  difficult  and  unsatisfac- 
tory. If  close  scrutiny  fails  to  detect  cardiac  impulse,  this  must 
not  necessarily  be  attributed  to  feebleness  of  the  impulse ;  it  may 
be  due.  to  the  intervening  layer  of  adipose  tissue. 

Palpation. — For  the  same  reason  the  hand  laid  upon  the  chest 
fails  to  locate  the  apex-beat,  or  indeed  to  perceive  any  cardiac 
shock  whatever.  The  real  value  of  palpation,  therefore,  is  in  the 
study  of  the  pulse,  which  should  be  carefully  studied  for  any  in- 
formation it  may  afford.  If  it  is  of  good  strength  and  volume  and 
in  rate  is  stable  and  not  unduly  accelerated,  it  points  to  a  fairly 
healthy  heart-muscle.  If,  on  the  contrary,  the  peripheral  arteries 
are  thick — a  matter  which  the  corpulence  often  renders  by  no 
means  easy  of  determination — if  the  pulse  is  unsteady  and  per- 
haps intermittent,  then  it  is  likely  that  chronic  myocarditis  is 
present  or  that  the  muscle-fibres  have  suffered  atrophy  from  possi- 
ble encroachment  upon  them  by  the  excessive  deposit  of  fat.  Pal- 
pation of  the  liver  with  a  view  to  ascertaining  if  this  organ  is  en- 
larged, is  also  a  matter  of  great  difficulty  and  even  impossibility, 
in  consequence  of  the  size  and  resistance  of  the  corpulent  abdomen. 
Even  if  the  liver  is  palpable,  this  may  be  due  to  its  being  fatty, 
and  not  to  a  state  of  passive  congestion. 

Percussion. — This  means  of  investigation,  upon  which  so 
much  reliance  is  ordinarily  placed  for  the  detection  of  cardiac 
enlargement,  is  of  but  small  aid  in  the  obese,  for  reasons  that  lie  in 
their  corpulence.     There  is  often  a  development  of  fat  within  the 


FATTY   HEART  '  605 

mediastinum  which  gives  an  area  of  diilness  that  may  be  thought 
to  belong  to  the  heart,  yet  in  reality  does  not.  Furthermore,  the 
mass  of  fat  within  the  omentum  and  upon  the  abdominal  walls  im- 
pedes the  descent  of  the  diaphragm,  if  it  does  not  actually  crowd 
it  upward,  and  thus  cause  the  heart  to  assume  an  abnormally  high 
and  horizontal  position.  When  this  is  the  case  the  area  of  cardiac 
dulness  is  increased  transversely  and  upward,  giving  a  false  ap- 
pearance of  increased  size  of  the  organ.  Consequently  extreme 
care  is  necessary  in  drawing  any  conclusion  from  an  increase  of 
pr£ECordial  dulness.  If,  however,  by  percussion  in  the  various 
ways  described  in  the  introductory  chapter  one  becomes  satisfied 
that  such  an  increase  does  not  exist,  it  affords  presimaptive  evi- 
dence that  the  symptoms  are  due  to  potential,  not  structural  in- 
competence. 

Auscultation. — This  is  likely  to  afford  the  best  evidence  of  the 
real  state  of  the  heart,  and  yet  we  know  that  the  muscle  may  be 
seriously  diseased  without  any  appreciable  change  in  the  heart- 
sounds.  If  these  are  found  to  be  only  rather  distant  and  feeble 
but  still  clear,  and  the  aortic  second  sound  of  good  relative 
strength,  it  is  in  favour  of  the  integrity  of  the  heart-muscle  being 
still  preserved.  If,  on  the  contrary,  the  first  sound  is  disproportion- 
ately feeble,  perhaps  impure  or  even  obscured  by  a  systolic  apex- 
murmur,  if  the  aortic  second  sound  is  weak  and  the  pulmonic  sec- 
ond unduly  loud,  there  is  reason  to  believe  the  heart  is  enlarged. 
This  may  be  a  simple  hypertrophy  with  dilatation,  or  there  may 
be  in  addition  myocardial  degeneration.  Physical  examination 
alone  does  not  enable  us  to  decide ;  we  must  endeavour  to  deter- 
mine this  point  by  the  study  of  all  those  factors  outside  of  the 
heart  which  make  for  or  against  cardio-vascular  decay. 

Diagnosis. — It  is  not  a  difficult  matter  to  diagnose  cardiac 
inadequacy.  The  real  problem  to  solve  is  whether  the  heart  is 
only  potentially  unequal  to  its  work  or  is  incompetent  in  conse- 
quence of  fatty  overgrowth  or  of  myocardial  disease.  If  the  pulse 
is  normal  in  rate  and  quality,  and  if  subjective  symptoms  are  felt 
only  upon  exertion,  are  slight  and  quickly  subside  after  cessation 
of  effort,  the  heart-walls  are  presumably  intact.  This  conclusion 
is  strengthened  if  minute  inquiry  fails  to  elicit  history  of  cardiac 
strain,  acute  infectious  disease,  bad  habits,  or  any  other  influence 
that  may  serve  to  impair  the  integrity  of  the  myocardium.    On  the 


606  DISEASES   OF   THE   HEART 

other  hand,  degenerative  changes  are  probable  if  the  patient  is 
past  middle  age,  if  the  pulse  shows  notable  alteration  in  quality 
and  rhythm,  and  if  symptoms  of  inadequacy  are  present  even  when 
the  patient  is  at  rest  or  not  making  unwonted  denumds  on  his 
heart.  If  the  individual  belongs  to  the  category  of  fat  and  anae- 
mic, the  heart-muscle  is  likely  to  be  flabby  and  its  incompetence  to 
be  due  to  dilatation.  If,  on  the  contrary,  symptoms  of  inadequacy 
develop  in  the  fat  and  plethoric,  whose  skeletal  muscles  are  firm 
and  large  and  whose  weight  is  due  to  the  great  specific  gravity  of 
their  muscles,  bones,  organs,  etc.,  and  not  to  adipose  tissue,  it  may 
reasonably  be  concluded  that  the  heart  is  overstrained,  perhaps 
dilated,  but  not  hampered  by  deposit  upon  it  of  fat. 

Finally,  if  symptoms  of  cardiac  incompetence  develop  in  any 
corpulent  person  it  is  the  part  of  wisdom  to  make  a  diagnosis  of 
cardiac  inadequacy  and  not  of  fatty  heart,  for  we  possess  no  means 
of  determining  during  life  whether  there  is  or  is  not  an  excessive 
dei)()sit  of  fat  within  the  heart-muscle. 

Prognosis. — This  depends  upon  the  condition  which  is  re- 
sponsible for  the  embarrassment  of  circulation.  If  the  patient 
is  young  and  muscular  and  the  cause  of  the  heart-weakness  is 
found  to  lie  in  potential,  not  structural  disability,  or  if  the  symp- 
toms date  from  some  recent  cardiac  strain,  the  heart-muscle  having 
been  previously  competent,  the  prognosis  is  comparatively  favour- 
able, since  appropriate  treatment  may  restore  compensation.  If, 
on  the  other  hand,  the  patient's  musculature  is  flabby,  he  is  anae- 
mic, and  gives  a  history  of  indolent  habits ;  if  his  symptoms  have 
steadily  increased,  and  especially  if  their  gravity  indicates  a  seri- 
ous breakdown  of  the  heart — then  there  is  but  small  hope  of  rein- 
stating compensation,  and  death  is  only  a  question  of  time.  An- 
gina pectoris,  attacks  of  asthma,  thickened  arteries  with  high 
sustained  pulse-tension,  likewise  furnish  a  hopeless  prognosis  as 
regards  recovery.  The  j^robable  duration  of  the  malady  cannot  be 
stated  with  any  accuracy,  but  the  course  is  likely  to  be  a  short  one. 
In  other  respects,  prognosis  is  governed  by  the  same  conditions 
as  in  otlicr  tOnns  of  heart-disease. 

Treatment. — It  is  essential,  in  the  correct  management  of 
any  dis(!ase,  that  the  physician  have  a  clear  knowledge  of  its  pa- 
thology and  of  the  object  to  be  attiniicd  by  treatment.  If  by  the 
term  "  fatty  heart "  were  meant  simply  a  heart  overgrown  and 


FATT¥   HEART  60Y 

infiltrated  with  adipose  tissue,  then  the  plain  indication  of  treat- 
ment would  be  the  absorption  of  excessive  fat,  and  the  object 
would  be  accomplished  by  putting  the  patient  upon  a  regime  cal- 
culated to  reduce  his  obesity.  In  this  chapter,  however,  the  dis- 
ease has  been  considered  from  a  diiferent  standpoint.  It  has 
been  looked  upon  as  a  condition  of  potential  weakness,  the  heart 
becoming  relatively  inadequate  to  the  requirements  of  the  circula- 
tion, rendered  necessary  by  the  size  of  the  body.  There  may  or 
may  not  be  an  undue  deposit  of  fat  upon  the  heart  itself.  This 
being  the  pathology  of  the  disease,  the  indication  is  to  restore  or 
establish  a  proper  relation  between  cardiac  power  and  body  weight. 
This  is  to  be  accomplished  by  measures  that  will  either  invigorate 
the  heart-muscle  without  reduction  of  the  obesity,  or  will  bring 
about  the  latter  without  the  former,  or  will  do  both.  By  the  pa- 
tient, it  is  generally  thought  that  the  reduction  of  his  corpulence 
is  all  that  is  necessary ;  but  Romberg  repeatedly  utters  an  em- 
phatic warning  against  such  an  idea.  He  states  again  and  again 
that  harm  rather  than  benefit  is  likely  to  follow  the  indiscriminate 
employment  of  the  ordinary  anti-fat  cures,  since  they  increase  the 
already  existing  heart-weakness.  The  need  of  such  a  warning 
was  forcibly  impressed  upon  me  only  this  past  winter. 

A  corpulent  man  of  fifty-five,  who  had  yet  been  able  to  exer- 
cise without  sjDccial  discomfort,  concluded  he  would  try  a  reduc- 
tion-cure at  Marienbad,  Germany.  By  vigorous  use  of  the  waters 
and  an  unreasonable  amount  of  walking  he  reduced  his  weight  45 
pounds  in  a  few  weeks  and  returned  home  feeling,  as  he  said, 
"  fine."  jSTevertheless,  he  had  not  been  home  long  when,  on  at- 
tempting to  walk  to  his  place  of  business  one  morning  as  usual, 
he  was  seized  with  great  shortness  of  breath,  that  compelled  him 
to  return  to  the  house.  This  was  the  beginning  of  the  end,  for  he 
failed  steadily  in  spite  of  the  most  approved  treatment,  and  died 
in  less  than  six  months. 

Depleting  measures  should  be  confined  to  cases  in  which  circu- 
latory disturbance  is  attributable  to  obesity  and  not  to  cardiac 
insufficiency.  Such  cases  are  found  for  the  most  part  in  persons 
who  are  still  young,  or  have  not  yet  passed  the  age  of  forty.  It  is 
often  a  matter  of  great  difficulty  to  determine  whether  the  trouble 
resides  in  the  heart  or  not,  and  therefore  an  anti-obesity  plan  of 
treatment  should  not  be  decided  on  hastily  or  without  thoughtful 


608  DISEASES  OF   THE   HEART 

study  of  all  those  considerations  bearing  on  this  point.  Should 
this  plan  of  management  be  at  length  decided  upon,  the  effect 
on  the  heart  should  be  carefully  watched  and  the  treatment  dis- 
continued altogether,  or  the  weight  reduction  carried  on  less  vigor- 
ously, so  soon  as  debility,  nervousness,  and  other  signs  of  cardiac 
or  general  asthenia  make  their  appearance. 

It  is  of  importance  also  what  system  of  dietary  is  selected. 
There  are  several  well-known  anti-fat  dietaries,  such  as  Banting's, 
Ebstein's,  Oertel's,  and  Sweninger's,  but  they  all  have  the  one  fea- 
ture in  common,  that  they  greatly  restrict  the  consumption  of  car- 
bohydrates. Their  chief  differences  are  in  the  amount  of  albumin 
and  fat  allowed.  Ebstein  permits  much  less  albumin  and  far  more 
fat  than  do  the  others,  while  the  Oertel  system  allows  considerably 
more  albumin  and  far  less  fat,  and  again  more  carbohydrates. 
They  all  restrict  the  consumption  of  fluids.  Whatever  differences 
they  possess,  they  all  attain  their  end  by  causing  an  absorption  of 
fat,  both  by  the  taking  away  of  fat-forming  food  and,  with  the 
exception  of  Ebstein's,  by  the  administration  of  a  relatively  large 
proportion  of  albumin,  which  is  thus  said  to  stimulate  the  absorp- 
tion of  fat.  In  addition  to  restricting  the  diet,  exercise  is  insisted 
upon  and  saline  cathartic  waters  are  administered. 

The  great  objection  to  the  employment  of  such  a  regime  in 
cases  of  so-called  fatty  heart  lies  in  the  fact  that  unless  the  indi- 
vidual is  capable  of  considerable  exercise,  whereby  adipose  tissue 
may  be  oxidized,  the  obesity  will  only  yield  when  the  diet  is  so 
strict  as  to  become  practically  a  starvation  diet.  It  is  a  well- 
known  principle  underlying  the  dietary  of  heart-disease,  that  in- 
asmuch as  the  heart-muscle  performs  an  enormous  amount  of 
work,  it  should  receive  a  relatively  large  proportion  of  proteid — 
i.  e.,  tissue-forming  food — and  must  under  no  circumstances  be 
deprived  of  adequate  nourishment.  Consequently,  if  an  attempt 
is  to  be  made  to  diminish  the  corpulence  of  a  person  with  cardiac 
insufficiency,  a  dietary  must  be  selected  that  will  most  nearly 
meet  the  demands  of  the  heart.  This  is  undoubtedly  tlie  one  se- 
lected by  Oertel,  while  the  Ebstein  and  Banting  systems  are  clearly 
inadmissible.  The  daily  allowance  of  the  several  elements  permit- 
ted by  Oertel  are  as  follows:  All)iniiiii,  t)l  oinices;  fats,  1  to  1| 
ounces;  carbohydrates,  2\  to  o^  ounces.  For  ])articulars  tlu;  reader 
is  referred  to  Oertel's  original  work,  or  to  treatises  on  dietetics. 


FATTY  HEART  609 

In  carrying  out  a  diet  for  the  reduction  of  obesity  in  the  class 
of  cases  now  under  consideration,  it  is  very  unsafe  to  produce  a 
too  rapid  loss  of  weight.  In  my  opinion  this  should  not  exceed 
2,  or  at  the  very  outside  3  pounds  a  week,  and  in  many  cases  1 
pound  is  better.  Consequently  the  physician  should  keep  an  accu- 
rate record  of  the  weight,  and  many  times  will  have  to  modify  the 
diet  given  above  by  increasing  the  albumin  or  starches,  or  both. 
If  the  physician  is  in  doubt  concerning  the  actual  state  of  the 
heart-muscle,  or  if  the  patient  finds  he  is  unable  to  take  adequate 
exercise,  then  massage  will  often  be  found  of  great  service  by 
promoting  oxidation  of  adipose  tissue.  It  also  aids  the  circu- 
lation. 

The  daily  use  of  laxative  waters  is  essential,  and  Germain 
See  recommends  the  administration  in  moderate  doses  (5  to  10 
grains)  of  iodide  of  potassium  three  times  a  day. 

For  the  past  few  years  the  public  and  profession  have  heard 
much  concerning  the  efficacy  of  reducing  fat,  of  the  alternate 
daily  use  of  Vichy  and  Kissingen  waters.  From  my  rather  lim- 
ited observation  of  their  efl^ects,  I  am  inclined  to  the  opinion  that 
if  these  waters  are  to  prove  efficient  they  must  be  combined  with 
exercise  and  at  least  a  moderate  restriction  in  the  consumption  of 
carbohydrates. 

In  elderly  people,  or  those  with  feeble  muscular  development, 
or  in  such  as  already  display  pronounced  symptoms  of  cardiac 
inadequacy,  energetic  treatment  for  the  reduction  of  corpulence 
is  hazardous,  to  say  the  least.  In  many  instances  the  weakness 
of  the  heart  will  be  intensified.  Romberg  is  of  the  opinion  that 
such  persons  should  not  be  subjected  to  the  possible  dangers  of 
such  treatment;  while  to  make  a  routine  practice  of  depleting  all 
fat  patients  certainly  cannot  be  too  strongly  condemned.  ]^ever- 
theless,  I  believe  in  most  cases,  even  when  the  heart  is  primarily 
at  fault,  some  modification  of  the  diet  will  usually  prove  bene- 
ficial. Some  of  these  patients  are  anaemic  as  well  as  corpulent — 
some  because  they  have  been  light  feeders  for  years,  others  be- 
cause they  have  habitually  taken  too  little  albumin  and  too  much 
starch  and  sugar,  while  still  others  have  consumed  altogether  too 
much  fluid,  particularly  at  meal-time. 

In  the  first  class,  attempt  should  be  made  to  secure  more  ade- 
quate nourishment  through  medicinal  or  other  measures  calcu- 
40 


610  DISEASES  OF   THE   HEART 

lated  to  improve  the  appetite  and  assimilation.  To  this  end  sim- 
ple bitters  and  tonics — as  quassia,  gentian,  iron,  nux  vomica, 
arsenic,  or  the  hypoplios})hites — may  be  tried,  together  with  acids, 
pepsin,  pancreatin,  and  kindred  preparations.  A  cupful  of  hot 
water  half  an  hour  before  each  meal  often  improves  both  appetite 
and  digestion.  In  quality  the  meals  should  be  highly  nutritious, 
so  that  in  quantity  they  may  be  light.  This  may  be  accomplished 
by  the  adcUtion  of  the  expressed  juice  of  fresh  beef,  or  by  some 
one  of  the  prepared  foods  rich  in  nitrogen  and  fat  but  poor  in 
carbohydrates. 

For  the  second  class  it  can  do  but  little  harm  to  reduce  starches 
and  sugar  and  increase  the  animal  food,  without,  however,  con- 
forming strictly  to  the  amount  and  proportion  laid  down  in  rigid 
anti-fat  dietaries.  In  the  last  class  it  may  be  sufficient  to  dimin- 
ish the  ingestion  of  fluids  without  otherwise  curtailing  or  modify- 
ing the  food  allowance. 

In  all  individuals  who  display  more  or  less  heart-weakness 
the  important  point  in  the  management  must  be  the  attempt  to  re- 
invigorate  the  heart.  If  its  load  cannot  be  lightened — that  is,  if 
the  corpulence  cannot  be  reduced — efforts  to  strengthen  the  heart 
are  likely  to  prove  futile.  The  physican  will  then  have  to  choose 
one  or  the  other  alternative ;  either  to  persevere  in  his  futile 
attempt  to  rehabilitate  the  heart,  or  to  run  the  risk  of  reducing  the 
body  weight.  The  wise  thing  will  be  to  try  to  accomplish  both. 
It  may  be  that  the  loss  of  half  a  pound  or  a  pound  a  week  will 
not  materially  weaken  the  patient,  and  yet  may  be  sufficient  to 
greatly  aid  the  doctor's  efforts  towards  re-establishing  cardiac 
power. 

By  all  odds,  the  best  means  to  this  end  is  exercise.  This  should 
be  limited  to  two  kinds — easy  walking  and  resistance  gymnastics. 
Kules  for  the  latter  have  already  been  given  (see  page  455).  The 
conditions  that  are  to  control  tlie  daily  walk  should  be  carefully 
laid  down  by  the  physician.  (1)  Walking  should  be  done  from 
one  to  four  hours  after  meals,  according  to  the  degree  of  cardiac 
debility.  (2)  The  walk  should  not  be  so  prolonged  as  to  occa- 
sion fatigue,  and  of  course  must  vary  greatly  in  individual  cases. 
The  medical  adviser  will  have  to  determine  its  length  by  observ- 
ing tlie  immediate  effect  of  exercise,  or  l)y  a  searching  inquiry  as 
to  symptoms.      ('^)  The  ])ac('  ninst  not  be  fast  enough  to  cause 


FATTY   HEART  611 

shortness  of  breath  or  palpitation,  and  it  is  always  best  to  begin 
very  slowly,  the  gait  to  be  quickened  only  as  the  exercise  produces 
a  feeling  of  well-being  or  lightness  in  the  chest.  (4)  The  patient 
must  not  walk  against  a  strong  wind,  and  must  confine  his  exercise 
to  level  ground,  Attemj^ts  to  carry  out  the  Oertel  system  of  as- 
cending an  incline  are  not  to  be  permitted  until  a  considerable 
degree  of  compensation  has  been  established.  If  the  patient  is 
exceptionally  intelligent  and  his  judgment  can  be  relied  upon,  it 
may  be  safe  to  allow  him  a  little  latitude  in  this  regard ;  but 
patients  are  more  likely  to  do  themselves  harm  by  essaying  paths 
that  are  too  steep,  than  they  are  to  derive  benefit  from  accustoming 
themselves  to  ascending  gentle  acclivities.  Therefore  in  a  large 
majority  of  instances  the  fourth  rule  should  be  strictly  insisted 
upon. 

When  heart-weakness  has  reached  such  a  degree  that  walking 
even  about  the  room  occasions  decided  dyspnoea,  there  is  no  pros- 
pect of  improvement  from  exercise,  and  life  will  probably  be  pro- 
longed by  keeping  the  patient  "quiet  and  relying  on  skilful  massage 
or  very  carefully  conducted  gymnastics.  Another  highly  useful 
and  often  very  promising  measure  for  restoration  of  heart-power 
is  the  balneological  treatment — i.  e.,  saline  baths  as  given  at  Bad 
l^auheim  and  already  described.  In  the  hands  of  one  experi- 
enced in  their  use  these  baths  are  rarely  likely  to  do  harm,  except 
in  those  cases  in  which  dilatation  has  become  extreme,  or  other 
contra-indications  are  present. 

Among  therapeutic  measures  are  included  also  the  ordi- 
nary heart-tonics,  such  as  digitalis,  strophanthus,  and  their  con- 
geners, as  well  as  strychnine  and  cardiac  stimulants,  nitroglyc- 
erin, ammonia,  camphor,  and  valerian.  The  same  rules  govern 
their  administration  in  these  as  in  other  cases  of  cardiac  insuffi- 
ciency from  whatever  cause.  Romberg  is  of  the  opinion  that  but 
little  good  is  to  be  expected  from  digitalis ;  but  in  my  opinion,  if 
its  vaso-constrictor .  efi^ects  can  be  counteracted  by  nitroglycerin 
or  iodide  of  potassium,  the  remedy  should  theoretically  support 
the  failing  heart  in  cases  of  obesity,  as  well  as  in  any  other  non- 
valvular  disease.  If  pulse-tension  is  persistently  high,  strophan- 
thus may  be  of  use,  either  alone  or  combined  with  digitalis  and 
strychnine.     The  last-named  heart-tonic  should  never  be  omitted. 

In  all  cases  of  obesity  blood-pressure  is  high  within  the  ab- 


612  DISEASES  OF  THE  HEART 

dominal  vessels,  and  therefore  I  firmly  believe  that  if  any  results 
are  to  be  attained  from  the  use  of  heart-tonics,  or  indeed  from 
other  measures,  as  exercise  and  baths,  tension  within  the  abdomen 
must  be  lessened  by  the  persistent  use  of  cathartic  remedies. 
Both  because  of  the  tendency  of  alkalies  to  reduce  weight,  and 
on  account  of  their  non-irritating  properties,  the  cathartic  selected 
should  be  a  saline  aperient  water — Hunyadi,  Rubinat-Condal, 
Concentrated  Pluto,  Apenta,  Franz  Josef,  Carlsbad,  or  any  other 
of  the  well-known  aperient  waters  on  the  market.  Care  should 
be  had  not  to  produce  weakness  by  a  strongly  purgative  efPect  each 
day,  but  only  to  keep  the  stools  semi-liquid  and  copious. 

It  is  usually  well  to  introduce  a  dose  of  calomel  or  blue  pill 
occasionally  at  bedtime.  The  compound  infusion  of  senna,  which 
is  only  the  old  English  "  Black  Draught,"  4  ounces  of  which  may 
be  taken  at  a  time,  forms  a  capital  purgative  for  occasional  use. 

Special  management  is  required  by  complications,  as,  for  ex- 
ample, the  use  of  iodide  of  potash  or  soda  in  chronic  arteriosclero- 
sis, sometimes  observed  in  obese  patients,  nitroglycerin  and  mor- 
phine in  cases  of  angina  pectoris  or  cardiac  asthma.  When  at 
last  cardiac  power  is  utterly  lost,  diuretin-Knoll  may  be  of  service 
in  reducing  dropsy,  or  at  least  holding  it  in  check.  Overdisten- 
tion  of  the  cardiac  cavities,  particularly  the  right  chamber,  may 
be  temporarily  relieved  and  the  patient's  suffering  ameliorated  by 
venesection.  Owing  to  the  associated  anaemia,  the  amount  of 
blood  thus  abstracted  should  be  small,  6  to  12  ounces  being  usually 
sufficient  to  render  the  pulse  soft  and  full.  Other  measures  for 
the  relief  of  the  patient  must  be  left  to  the  physician's  judgment 
and  to  the  special  indication  of  each  case. 


CHAPTER  XXIV 

CARDIAC   ASTHMA— CHEYNE-STOKES    RESPIRATION- 
BRADYCARDIA-STOKES-ADAMS  SYNDROME 

In   this   and   the   succeeding  chapter   are  considered   certain 

phenomena   that    are    sometimes    encountered    in   the   course    of 

myocardial  disease,  and  in  the  opinion  of  the  author  may  not 

inappropriately  be  discussed  in  connection  with  disorders  of  the 

myocardium. 

I.    CARDIAC  ASTHMA 

!No  one  symptom  is  so  frequently  a  feature  of  cardiac  disease 
as  dyspnoea,  and  with  the  possible  exception  of  prsecordial  pain 
there  is  no  subjective  disturbance  so  distressing.  In  many  in- 
stances, moreover,  it  occasions  such  obvious  suffering  as  to  be 
actually  harrowing  to  the  spectator.  True  cardiac  dyspnoea  is  due 
to  the  swelling  and  rigidity  of  the  lungs  caused  by  stasis  within 
them,  and  consequently  forms  an  important  part  of  the  clinical 
picture  in  most  cases  of  cardiac  inadequacy. 

It  would  be  a  mistake,  however,  to  attribute  the  dyspncea  of 
cardiopaths  solely  to  circulatory  embarrassment.  Thus  it  may  be 
due  to  pain,  in  consequence  of  which  the  individual  fears  to 
breathe  with  his  customary  depth  and  slowness.  In  other  cases 
it  may  result  from  nervousness  or  apprehension,  as  e.  g.,  during 
an  examination  of  the  heart.  In  all  such  instances,  however,  it  is 
usually  easy,  by  giving  due  consideration  to  the  state  of  the  circu- 
latory apparatus,  to  recognise  the  true  cause  of  the  breathlessness. 

Cardiac  dyspnoea  is  par  excellence  a  dyspnoea  of  effort — i.  e., 
it  is  either  evoked  by  exertion  or  intensified  by  the  same.  This 
breathlessness  of  effort  may  be  regarded  as  the  earliest  manifes- 
tation of  failing  heart-power,  and  so  long  as  cardiac  incompe- 
tence is  of  minor  degree,  is  confined  to  periods  of  physical  exer- 
tion. There  nearly  always  comes  a  time,  however,  when  dysp- 
noea becomes  more  or  less  constant  even  during  rest  and  when 
apparently  trivial  conditions  intensify  the  shortness  of  breath 
even  to  the  point  of  positive  air-hunger.     This  has  been  repeatedly 

613 


G14  DISEASES   OF   THE   HEART 

dwelt  upon  in  foregoing  pages  in  considering  the  manifestations 
of  valvular  disease. 

Persons  suffering  from  myocardial  inadequacy  of  whatever 
cause  also  display  dyspnoea  of  effort  quite  like  that  of  other  cardio- 
paths,  and  likewise  due  to  circulatory  emharrassment. 

There  is  a  form  of  dyspncea  displayed  by  these  patients,  how- 
ever, which  is  so  intense  and  paroxysmal  that  it  has  not  inaptly 
been  termed  cardiac  asthma.  As  implied  by  the  name,  it  closely 
resembles  an  attack  of  bronchial  asthma.  In  most  cases  it  is  not 
a  growing  intensification  of  already  existing  dyspnoea,  but  is  a 
more  or  less  sudden  attack  of  such  distressing  shortness  of  breath 
as  to  constitute  veritable  orthopncea  for  the  time. 

The  attack  may  be  induced  by  effort,  but  in  its  most  typical 
form  it  comes  on  at  night.  It  is  therefore  a  nocturnal  dyspnoea. 
The  attack  may  seize  the  individual  so  soon  as  he  lies  down  at 
night,  but  frequently  it  does  not  appear  until  after  he  has  been 
asleep  for  a  few  hours.  The  jiatient  is  then  aroused  b}^  a  sense  of 
oppression  or  want  of  sufficient  air,  which  obliges  him  to  sit  up  or 
arise  and  walk  slowly  about  his  apartment. 

In  its  mildest  manifestations  this  is  all,  but  generally  the 
dyspnoea  is  far  more  severe.  The  shortness  of  breath  increases 
until  in  a  few  minutes,  occasionally  from  the  very  start,  the  suf- 
ferer is  forced  to  breathe  with  great  rapidity  and  difficult}'.  His 
chest  emits  a  multitude  of  fine  or  coarse  moist  nlles  due  to  intense 
pulmonary  congestion  and  transudation  of  serum  into  the  air- 
tubes,  and  the  consequent  cough  is  attended  with  the  expectora- 
tion of  frothy  or  even  bloody  mucus. 

The  patient's  distress  is  now  terrible  both  to  himself  and 
friends,  his  face  becomes  cyanosed  and  bedewed  with  perspira- 
tion, while  his  pulse  is  rapid,  extremely  feeble,  and  even  irregular 
or  intermittent.  If  the  heart  is  now  examined  it  is  found  to  be 
dilated,  while  its  sounds  are  extremely  faint,  partly  in  conse- 
quence of  the  rales  of  pulmonary  a'dema,  but  mainly  because  of 
cardiac  weakness. 

Such  an  attack  may  last  for  minutes  or  even  hours,  yet  with 
scarcely  the  initial  severity.  As  a  rule  it  :d)ates  in  from  fifteen 
to  thirty  minutes.  With  cessation  of  the  terrific  dyspnoea  the 
sufferer  is  left  exhausted  and  usually  in  a  state  of  great  mental 
agitation. 


CHBYNE-STOKES  RESPIRATION  615 

The  cause  of  this  cardiac  asthma  is  believed  to  be  temporary 
weakness  of  the  left  ventricle  and  disproportionate  strength  of  the 
right  ventricle.  This  condition  on  the  part  of  the  two  ventricles 
leads  to  congestion  of  the  lungs  and  consequent  dyspnoea.  As  the 
stasis  increases  and  pulmonary  oedema  occurs,  dyspnoea  becomes 
increased  in  consequence  of  mechanical  interference  with  oxy- 
genation of  the  blood.  Certainly  such  an  explanation  fits  the  clin- 
ical manifestations  of  an  attack. 

The  predisposition  to  cardiac  asthma  is  furnished  by  degener- 
ation and  enfeeblement  of  the  left  ventricle,  while  the  immediate 
or  exciting  cause  may  be  found  in  whatever  temporarily  overpow- 
ers the  ventricle — i.  e.,  undue  physical  effort.  Coitus,  by  reason 
of  the  union  of  both  effort  and  excitement,  seems  particularly  apt 
to  excite  an  attack.  The  occurrence  of  the  attack  after  some  hours 
of  sleep  is  thought  to  be  explained  by  the  augmentation  of  blood- 
pressure  said  to  be  incident  to  the  recumbent  posture.  Huchard 
states  that  blood  pressure  is  increased  by  the  recumbent  position, 
while  Gaertner,  on  the  other  hand,  claims  that  his  tonometer  shows 
an  actual  though  slight  decrease  of  pressure.  If  this  is  so,  some 
other  explanation  is  required  for  the  occurrence  of  cardiac  asthma 
during  sleep.  This  may  be  found  in  the  added  work  put  upon  the 
left  ventricle  in  maintaining  blood-flow  by  muscular  inaction,  and 
the  more  quiet  respiration  incident  to  sleep. 

It  is  needless  to  remark  that  such  attacks  are  highly  dangerous 
and  call  for  prompt  and  energetic  treatment.  To  this  end  stimu- 
lants are  indicated,  and  nothing  is  so  efficient  as  the  hypodermic 
injection  of  ^  of  a  grain  of  morphine  combined  with  the  atropine 
found  in  the  ordinary  hypodermic  tablet. 

II.   CHEYNE-STOKBS  RESPIRATION 

This  is  a  rhythmical  form  of  dyspnoea,  first  carefully  described 
by  the  two  eminent  physicians  whose  names  are  now  inseparably 
linked  with  this  distressing  symptom.  It  is  characterized  by  alter- 
nating periods  of  dyspnoea  and  apnoea,  which  recur  at  regular  in- 
tervals and  supplant  normal  breathing. 

The  phenomena  of  this  type  of  respiration  may  be  described 
as  follows :  After  a  period  of  suspended  breathing  or  apnoea,  res- 
pirations return,  at  first  slowly  and  superficially,  each  succeeding 
one  quicker  and  deeper,  until  at  length  the  inspirations  become 


616  DISEASES  OF   THE   HEART 

strikingly  rapid  and  forcible,  and  maximum  dyspnoea  is  attained. 
After  having  maintained  this  height  for  a  few  seconds  the  respira- 
tory efforts  begin  to  abate  both  in  speed  and  depth,  dying  away 
gradually  into  another  period  of  complete  repose,  the  chest  being 
now  entirely  motionless.  After  this  stage  of  apnoea  has  lasted 
for  a  certain  number  of  seconds,  breathing  again  begins  in  the 
same  scarcely  perceptible  manner  to  wax  and  wane  as  before. 
Thus  cycle  after  cycle  is  repeated  with  perfect  regularity. 

The  duration  of  the  two  phases  that  constitute  an  entire  cycle 
or  paroxysm  differs  in  different  cases,  but  remains  constant  in  the 
same  case  after  this  form  of  dyspncea  has  become  well  established. 
It  is  not  very  uncommon  to  witness  incomplete  or  abortive  mani- 
festations of  this  peculiar  dyspnoea,  which  after  a  time  assume  the 
typical  Cheyne-Stokes  respiration.  Apnoea  usually  persists  for  a 
quarter  to  half  a  minute  and  the  period  of  dyspnoea  a  few  sec- 
onds longer.  In  12  cases  observed  by  Sansom  the  pause  varied 
in  duration  from  ten  to  forty  seconds  and  dj^spnoea  from  fifteen 
to  fifty-five  seconds.  In  one  case  he  noted  a  persistence  of  apnoea 
for  sixty  and  of  dyspnoea  for  sixty-five  seconds,  while  he  cites 
another  in  which  each  phase  continued  two  minutes.  During  the 
stage  of  respiratory  effort  the  ascending  and  descending  series 
endure  about  twenty  seconds  each,  while  the  acme  of  laboured 
breathing  continues  about  twenty-five  seconds  (Sansom).  The 
length  of  this  period — i.  e.,  of  dyspnoea — is  not  the  same  in  all 
cases,  however. 

Patients  exhibiting  Cheyne-Stokes  respiration  usually  retain 
consciousness  during  their  attacks  and  suffer  no  enfeeblcment  of 
their  mental  powers.  In  some,  on  the  contrary,  consciousness  is 
clouded  and  the  intellect  impaired. 

Certain  pupillary  phenomena  have  been  observed.  Thus  the 
pupils  are  contracted  during  apnoea  and  dilated  in  the  stage  of 
dyspnfX'a.  Finlayson  has  described  a  rhythmical  contraction  and 
dilatation  of  the  pupil  "  during  the  acme  of  the  respiratory  act," 
dilating  with  inspiration  and  contracting  with  expiration. 

Such  rhythmical  change  in  the  size  of  the  pupils  is  not  con- 
fined to  this  form  of  dyspnoea,  however,  for  a  similar  phenomenon 
has  been  observed  during  the  stertorous  breathing  of  coma. 

As  regards  the  pulse,  very  conflicting  observations  have  been 
recorded.     Some  observers  have  reported  perfect  uniformity  in 


CHEYNE-STOKES   RESPIRATION  617 

the  piilsc-rate  during  both  periods  of  the  cycle,  while  Little, 
quoted  by  Sansom,  witnessed  15  heart-beats  during  an  apnocal 
period  of  ten  seconds,  and  only  6  in  a  like  period  in  the  dyspnoeal 
stage.  Others  have  reported  retardation  of  the  pulse  durilig 
apna?a,  and  a  relative  acceleration  during  the  period  of  dyspnoea. 
Aside  from  changes  in  rhythm,  the  tension  of  the  pulse  is  said  to 
be  raised,  the  pulse  feeling  harder  and  firmer  than  normal. 

Diseases  in  which  Cheyne-Stokes  Breathing  is  Observed. — 
The  following  list  is  taken  from  Sansom's  work  on  the  Diagnosis 
of  the  Diseases  of  the  Heart  and  Thoracic  Aorta,  and  shows  that 
the  cases  in  which  this  form  of  dyspnoea  is  observed  are  by  no 
means  exclusivel}^  those  of  cardiac  disease.  (1)  Cases  attended 
with  cerebral  affections — viz.,  cerebral  haemorrhage,  tumours, 
tubercular  meningitis,  epilepsy,  shock  from  surgical  injury  with 
ura?mia,  alcohol  intoxication,  opium  poisoning,  and  insanity.  (2) 
Cases  attended  with  lesions  of  the  heart  and  great  vessels — viz., 
fatty  degeneration  of  the  heart,  pericarditis,  atheromatous  disease 
of  the  aorta,  aortic  aneurysm,  valvular  disease  (double  aortic, 
with  mitral  insufficiency,  mitral  stenosis,  dilatation  of  aorta  coex- 
isting, aortic  regurgitation  and  obstruction),  and  chronic  Bright's 
disease.  It  is  with  diseases  of  the  aorta  and  its  valves  that  it  is 
most  frequently  associated,  but  it  may  occur,  in  the  absence  of 
valvular  disease,  when  the  coronary  arteries  are  obstructed.  In 
any  of  these  conditions  it  is  most  probable  that  the  arteries  at 
the  base  of  the  brain  are  atheromatous,  and  the  concurring  af- 
fections of  the  heart  and  brain  speedily  lead  to  death.  (3)  Cases 
of  certain  acute  febrile  diseases^ — viz.,  diphtheria  (Hiitterbren- 
ner),  typhoid  fever  (Wharry),  puerperal  septicaemia,  scarlet 
fever,  pneumonia,  pertussis  (with  inanition),  and  influenza. 

Theories  to  Explain  Cheyne-Stohes  Respiration. — Before  giv- 
ing a  brief  statement  of  the  leading  theories  which  have  been 
advanced  to  explain  the  rhythmical  alteration  of  breathing,  it 
may  be  well  to  state  certain  physiological  facts  concerning  respira- 
tion. (1)  Inspiration  is  a  result  of  the  contraction  of  the  in- 
spiratory muscles  in  response  to  a  nervous  impulse  sent  out  from 
the  respiratory  centre  in  the  upper  portion  of  the  medulla  oblon- 
gata, close  to  the  calamus  scriptorius,  but  extending  to  the  upper 
portion  of  the  spinal  cord.  (2)  Expiration  is  for  the  most  part 
a  passive  act  due  to  the  elastic  resilience  of  the  lungs.      (3)   The 


618  DISEASES  OF  THE   HEART 

action  of  the  respiratory  centre  is  automatic  and  rhythmical.  (4) 
The  activity  and  energy  of  the  respiratory  centre  depend  in  great 
measure  upon  the  amount  of  oxygen  contained  in  the  blood,  and 
upon  the  amount  of  blood  supplied  to  the  centre.  It  is  not  difficult 
to  understand  why  there  may  be  dyspnoea  in  any  given  case,  but  it 
is  difficult  to  explain  why  the  dyspna'a  should  be  rhythmical  in 
the  way  characteristic  of  Cheyne-Stokes  breathing. 

The  first  attempt  to  explain  it  was  made  by  Traube,  and  is 
knoA\Ti  as  Trauhes  theory.  This  assumes  that  the  normal  excita- 
bility of  the  respiratory  centre  is  diminished  in  consequence  of  the 
supply  to  it  of  imperfectly  oxygenated  blood.  During  the  stage 
of  apnopa  carbonic  acid  accumulates  in  the  blood,  and  when  it 
has  become  excessive  begins  to  stimulate  the  respiratory  centre  to 
discharge  its  impulses.  In  response  to  these  discharges,  which 
are  at  first  slow  and  imperfect,  contraction  of  inspiratory  muscles 
takes  place,  grows  ever  deeper  and  more  rapid  until  at  length  the 
maximum  stage  of  dyspnoea  is  attained.  The  centre  now  ceases 
to  be  stimulated,  or  becomes  exhausted,  and  inspiratory  efforts 
gradually  decline  until  they  finally  terminate  in  the  stage  of  res- 
piratory pause  or  apncea.  Carbonic  acid  in  the  blood  is  again 
accumulated,  the  respiratory  centre  is  again  stimulated,  and  thus 
the  cycle  is  repeated  in  ever-recurring  paroxysms. 

Many  objections  have  been  urged  against  Traube's  theory,  but 
the  one  that  Bramwell  thinks  is  fatal  to  it  is  that  a  deficient  supply 
of  properly  oxygenated  blood  to  the  respiratory  centre  would 
stimulate  it  into  action  rather  than  impair  its  irritability,  since  it 
is  not  so  much  an  accumulation  of  carbonic  acid  as  a  want  of  oxy- 
gen in  the  blood  which  stimulates  the  respiratory  centre. 

To  explain  tlie  lowered  irritability  of  the  respiratory  centre, 
which  is  assumed  in  Traube's  theory,  Sansom  has  advanced  the 
proposition  that  the  centre  is  in  a  state  of  paresis  or  partial  paraly- 
sis in  consequence  of  some  cerebral  disease,  and  with  a  satisfactory 
explanation  of  the  diminished  excitability  of  the  respiratory  cen- 
tre Traube's  theory  would  then  become  complete. 

FileJine's  Theory. — This  assumes  tliat  liotli  the  vaso-motor  and 
respiratory  centres  are  concerned  in  the  j)n>(hu'ti()ii  of  this  form 
of  dyspncra.  According  to  his  explanation,  the  deficiency  of  oxy- 
gen and  excess  of  carbonic  acid  in  the  blood,  which  result  from 
the  period  of  apnosa,  stimulate  the  vaso-motor  centre,  and  the 


CHEYNE-STOKES   RESPIRATION  619 

arterioles  of  the  brain,  as  well  as  those  throughout  the  body,  become 
contracted.  This  constriction  of  the  arterioles  diminishes  the 
supply  of  blood  to  the  respiratory  centre,  and  in  consequence  this 
centre  is  stimulated  to  discharge,  and  inspiration  begins.  So 
soon,  however,  as  respiration  has  become  energetic  and  the  blood 
proj)erly  aerated,  stimulation  of  the  vaso-motor  centre  ceases,  arte- 
rial spasm  is  no  longer  maintained,  the  respiratory  centre  receives 
a  proper  supply  of  arterialized  blood,  and  dyspnoea  is  no  longer 
experienced.  The  respiratory  acts  gradually  die  away  and  the 
period  of  apnoea  is  again  reached.  There  again  occurs  stimulation 
of  the  vaso-motor  centre,  and  another  cycle  is  repeated.  Bram- 
well  is  of  the  opinion  that  if  Filehne's  theory  is  correct,  then 
Cheyne-Stokes  breathing  should  occur  much  more  frequently  than 
it  really  does.  He  says :  "  I  am  disposed,  therefore,  to  think  with 
Dr.  Sansom  that  something  more  is  necessary,  and  that  there 
must  be  some  alteration  of  the  respiratory  centre  itself  in  addition 
to  the  condition  which  Filehne's  theory  supplies.  A  state  of  irri- 
table weakness  would,  in  my  opinion,  account  for  this  condition." 
BramiDelV s  theory  in  explanation  of  Cheyne-Stokes  breathing 
is  based  on  the  supposition  that  the  respiratory  centre  consists  of 
two  parts : ,  an  inspiratory  and  an  expiratory,  and  that,  as  sug- 
gested by  Rosenthal,  "  the  inspiratory  centre  is  the  seat~  of  two 
conflicting  forces,  one  tending  to  generate  inspiratory  impulses, 
(the  discharging  portion  of  the  inspiratory  centre  as  we  may  call 
it),  and  the  other  offering  resistance  to  the  generation  of  these 
impulses  (the  restraining  or  inhibiting  portion  of  the  inspira- 
tory centre) — the  one  and  the  other  alternately  gaining  the  vic- 
tory, and  thus  leading  to  rhythmical  discharge."  Bramwell  as- 
sumes that  venous  blood  excites  the  discharging  portion,  restrains 
the  inhibiting  portion;  while  oxygenated  blood  depresses  the  for- 
mer portion,  and  intensifies  the  action  of  the  restraining  portion. 
If  the  discharging  portion  is  in  a  condition  of  irritable  weakness, 
and  therefore  more  easily  excited  to  discharge,  but  also  more 
quickly  and  easily  exhausted,  or  if  both  portions  are  in  a  condi- 
tion of  irritable  weakness,  then  there  is  a  condition  of  things, 
Bramwell  thinks,  which  satisfactorily  explains  the  phenomena  of 
Cheyne-Stokes  breathing.  At  the  end  of  apnoea  the  blood  is  highly 
venous,  and  therefore  gradually  excites  a  paroxysm  of  dyspnoea, 
by   stimulating  the   discharging   and   restraining   the   inhibitory 


620  DISEASES  OF   THE   HEART 

portion  of  the  centre.  In  the  second  place,  the  carbonic  acid  in 
the  blood  stinmlates  to  action  the  vaso-motor  centre,  the  arterioles 
become  contracted,  and  the  supply  of  oxygen  to  the  respiratory 
centre  is  still  further  diminished.  Furthermore,  the  irritable 
weakness  of  the  discharging  centre  causes  its  impulses  to  become 
excessive,  and  the  state  of  dyspna^a  results.  Moreover,  the  weak- 
ness of  the  discharging  portion  of  the  inspiratory  centre  causes  it 
to  become  quickly  overexhausted  and  the  dyspnoja  subsides.  In 
consequence  of  the  energetic  respiratory  effort  during  the  stage 
of  dyspna?a  the  blood  becomes  arterialized  and  the  discharging 
portion  of  the  inspiratory  centre  is  no  longer  stimulated,  but  the 
reverse  takes  place  as  regards  the  restraining  portion,  which  gains 
the  ascendency  over  the  weakened  and  exhausted  discharging  por- 
tion, and  the  state  of  apno3a  is  produced.  During  this  period  of 
rest  the  oxygenated  blood,  which  had  stimulated  the  restraining 
and  depressed  the  discharging  portion  of  the  inspiratory  centre  be- 
comes replaced  by  carbonic  dioxide ;  the  discharging  centre  is 
aroused  into  action  again,  and  the  inhibiting  is  restrained ;  inspir- 
atory efforts  are  renewed  and  another  cycle  is  repeated. 

Of  the  foregoing  theories,  conceived  to  account  for  this  distress- 
ing rhythmic  form  of  dyspna'a,  Bramwell's  is  the  most  satisfac- 
tory, and  yet,  as  he  himself  suggests,  it  is  difficult  to  explain  how 
this  condition  of  irritable  weakness  of  the  respiratory  and  vaso- 
motor centres  is  produced.  Bramwell  assumes  that  in  those  cases 
of  Cheyne-Stokes  breathing  displaying  a  contracted  pulse  and 
pallid  countenance,  there  is  local  anaemia  of  the  centres  in  conse- 
quence of  arterial  spasm,  and  irritable  weakness  takes  place. 

In  other  cases  not  showing  arterial  spasm  he  suggests  that  this 
unstable  state  of  the  centres  may  be  due  to  disease  within  the 
medulla  or  to  impressions  received  from  nervous  centres  situated 
higher  up  or  from  the  periphery,  especially  from  the  heart  or 
lungs,  through  the  agency  of  the  pneumogastric  and  superior  laryn- 
geal nerves.  Such  peripheral  stinndi  are  ])iirti('ularly  likely  to  be 
received  by  the  centres  in  those  cases  of  heart-disease  manifesting 
right-ventricle  dilatation  with  diminished  supply  of  blood  to  the 
lungs. 

Rosenhach's  Theory. — After,  as  he  states,  a  searching  analysis 
of  tlie  various  theories,  Rosenbach  has  adopted  the  following  ex- 
planation.     Under  the  influence  of  certain  anomalies  of  brain- 


CHEYNE-STOKES  RESPIRATION  621 

nutrition  there  develop  localized  disturbances  in  the  brain  or  in 
individual  centres,  particularly  in  that  of  respiration,  which  dis- 
turbances lessen  the  excitability  of  the  affected  part  and  augment 
the  normal  exhaustibility  of  the  same.  Thereby  are  produced 
remissions  in  the  activity  of  the  respective  centres  with  loss  of  tone 
in  the  vaso-motor  and  vagus  centres,  or  complete  intermissions, 
such  as  a  pause  in  the  respiratory  act,  with  a  kind  of  paralytic 
state  of  the  cerebrum,  manifested  by  a  periodic  sleep  with  contrac- 
tion of  the  pupils  and  movements  of  the  eyeballs.  So  soon  as  the 
fatigue  and  exhaustion  of  the  centre  have  disappeared  in  conse- 
quence of  cessation  of  respiration  and  an  augmented  internal  ac- 
tivity, and  its  excitability  returns,  respirations  again  set  in  and  con- 
tinue to  increase,  because  the  excitability  of  the  nervous  apparatus 
grows  out  of  proportion  or  waxes  more  rapidly  than  the  stimulus 
to  activity  wanes  in  consequence  of  organic  work.  So  soon  now  as 
the  abnormal  exhaustibility  of  the  centre  again  begins  to  be  felt, 
it  supersedes  the  stimulus,  and  therefore  the  functional  activity 
of  the  centre  lessens,  and  finally  ceases  altogether  when  at  last 
the  centre  has  become  completely  exhausted.  Whether  or  not  res- 
I^iration  takes  place  is  determined  by  the  ability  of  the  centre  to 
respond  to  stimulus,  and  the  depth  of  the  respiratory  act  depends 
not  upon  the  strength  of  the  impulse,  but  on  the  functional  capa- 
bility of  the  nervous  apparatus.  He  thinks  that  of  the  various 
nervous  centres  the  respiratory  is  the  one  that  suffers  most  readily 
and  often  alone,  while  the  vaso-motor  centre  is  relatively  much 
less  frequently  affected,  and  paralysis  of  this  means  death. 

He  furthermore  thinks  that  a  regularly  intermitting  pulse, 
pulsus  bigeminus  and  alternans,  may  be  a  manifestation  of'  peri- 
odicity in  the  function  of  the  vagus  and  vaso-motor  centres  in 
certain  cases  of  nutritional  disturbance  of  the  brain,  and  are  analo- 
gous to  the  Cheyne-Stokes  phenomenon.  As  Rosenbach  states,  this 
explanation  of  this  abnormal  type  of  breathing  differs  from  others 
in  the  assumption,  not  of  a  periodic  alteration  of  the  stimulus,  but 
in  a  rhythmic  change  in  the  excitability  of  the  centre  which  pre- 
sides over  respiration,  even  to  a  complete  abeyance  of  its  function 
for  the  time  being.  He  assumes  that  this  rhythmical  periodicity 
as  regards  excitability  is  to  be  referred  to  some  peculiar  charac- 
teristic inherent  in  the  nervous  apparatus  by  virtue  of  which  it  is 
capable  of  being  exhausted  and  again  aroused  to  activity. 


622  DISEASES  OF  THE   HEART 

It  is  needless  to  add  that,  however  ingeniously  the  pathology 
of  Cheyne-Stokes  respiration  may  be  speculated  upon,  the  subject 
is  still  enveloped  in  great  obscurity. 

Prognosis. — The  development  of  Cheyne-Stokes  breathing  is 
generally  held  to  be  of  unfavourable  significance,  by  indicating 
that  a  fatal  termination  is  not  far  off.  Yet  weeks  or  even  months 
may  sometimes  intervene  between  the  appearance  of  this  symptom 
and  death.  Murri  reported  a  case  in  which  the  phenomenon  per- 
sisted for  forty  days,  and  Sansom  one  for  one  hundred  and  eight 
days.  In  the  Lancet  of  April  5,  1890,  is  the  report  of  a  case  of  a 
man  of  ninety-two  who  manifested  the  symptom  for  several  years. 
This  type  of  dyspnoea  has  also  been  known  to'  appear,  then  cease, 
and  reappear  after  a  lapse  of  several  months.  In  most  of  the  cases 
that  recover,  or  in  which  the  symptom  is  greatly  protracted,  the 
disease  upon  which  it  dejiends  is  either  some  brain-lesion  or  an 
acute  affection,  as  influenza.  When  Cheyne-Stokes  breathing  is 
observed  in  cardiac  patients,  the  underlying  malady  is  itself  of  a 
grave  nature,  and  the  occurrence  of  this  symptom  usually  por- 
tends a  not  distant  termination  of  the  case.  To  this  rule  there  are 
exceptions,  however.  In  April,  1895,  I  was  consulted  by  an  old 
gentleman  of  eighty  who  manifested  this  symptom.  He  had  pro- 
nounced thickening  of  the  peripheral  arteries,  a  greatly  hypertro- 
j)hied  and  dilated  heart,  a  harsh  bruit  along  the  course  of  the 
aorta,  and  a  remarkably  intense  and  metallic  aortic  second  sound. 
In  addition  to  his  arteriosclerosis  and  myocardial  degeneration, 
his  liver  was  cirrhotic  and  the  urine  gave  evidence  of  chronic  in- 
terstitial nephritis.  Cheyne-Stokes  dyspnoea  was  typical,  and  in 
consequence  a  well-known  Chicago  consultant  had  given  a  sombre 
prognosis  on  the  ground  that  he  had  never  known  this  symptom 
to  endure  for  more  than  three  weeks  in  such  cases.  Yet  pari  passu 
with  iuiproveincnt  in  cardiac  tones  the  dyspncea  gradually  abated, 
and  after  about  two  weeks  was  entirely  lost,  never  again  to  return 
during  the  two  years  that  this  patient  was  spared  to  his  family. 

Another  gentlenuin  of  seventy-one  displayed  this  form  of 
breathing,  rather  irregularly  by  day  but  typically  by  night,  dur- 
ing the  time,  in  which  cardiac  asthenia  was  marked,  yet  recovered 
from  it  with  gradual  improvement  in  his  condition. 

It  has  seemed  t(»  nic  that  wlicii  ( 'hcync-Stokcs  respiration  is 
more  ])rononneed,  or  ])erchance  is  nuiniiVstcd  only  during  sleep, 


CHEYNE-STOKES  RESPIRATION  623 

it  is  not  of  so  grave  a  prognosis  as  when  present  with  equal  inten- 
sity both  waking  and  sleeping.  Miirri,  and  recently  Pembrie, 
have  called  attention  to  a  physiological  Cheyne-Stokes  respiration 
observed  in  healthy  persons  during  sleep.  But  the  patient  of  sev- 
enty-one was  not  healthy,  and  therefore  the  nocturnal  manifesta- 
tion of  Cheyne-Stokes  dyspnoea  during  his  periods  of  unconscious- 
ness in  sleep  could  not  be  regarded  as  physiological.  Finally,  the 
prognosis  must  be  looked  upon  as  specially  grave  in  those  cases 
which  also  manifest  obscuration  of  the  mental  faculties. 

Treatment. — When  Cheyne-Stokes  dyspnoea  is  a  symptom  of 
cardiac  disease  the  treatment  must  be  essentially  that  of  the  un- 
derlying condition.  Yet  we  are  called  on  to  mitigate  the  patient's 
distress  so  far  as  this  is  possible.  This  is  best  accomplished  by 
the  hypodermic  administration  of  morphine,  which,  if  it  does  not 
remove  the  dyspnoea,  blunts  the  patient's  sensibility.  The  value 
of  morphine  in  this  class  of  cases  has  been  the  subject  of  some 
contention  in  Germany.  At  the  meeting  of  the  Congress  for  In- 
ternal Medicine  at  Wiesbaden  in  1892,  Unverricht  read  a  paper 
in  which  he  expressed  the  decided  opinion  that  morphine  and 
atropine  are  powerless  for  the  removal  of  Cheyne-Stokes  breath- 
ing. Other  observers  have  gone  so  far  as  to  assert  that  morphine 
intensifies  rather  than  relieves  this  symptom.  Stadelmann  made 
25  observations  upon  the  effect  of  morphine  and  atropine,  alone  and 
combined,  upon  this  type  of  breathing.  The  observations  were 
made  upon  two  patients,  and  the  doses  were  0.01  to  0.02  (-|  to  -J) 
of  a  grain  of  morphine,  and  0.001  to  0.0015  (-^  to  ■£^)  of  a  grain 
of  atropine.  The  effects  were  neither  uniform  nor  constant. 
They  sometimes  shortened  the  period  of  apnoea,  sometimes  that  of 
dyspnoea,  and  at  other  times  they  lengthened  one  or  the  other  or 
both.  In  5  experiments  morphine  lessened  or  removed  the 
Cheyne-Stokes  respiration,  and  in  4  it  aggravated  the  symptom. 

Although  Stadelmann's  observations  were  so  inconstant  and 
unreliable  as  to  the  effect  of  morphine  that  they  seemed  to  con- 
firm Unverricht's  assertion,  he  nevertheless  concluded  that  on  the 
whole  the  effect  of  this  agent  was  to  mitigate  the  severity  of  the 
attack.  Morphine  certainly  seems  to  exert  no  injurious  effects ; 
and  since  it  undoubtedly  blunts  the  patient's  sensibility  and  in- 
duces sleep,  there  can  be  no  contra-indication  to  its  employment, 
even  if  it  seems  occasionally  to  change  an  irregular  or  unperiodic 


G24  DISEASES   OF   THE   HEART 

form  of  this  dyspna?a  into  the  periodic  rhythm  characteristic  of 
Cheyne-Stokes  respiration. 

A  word  of  caution  should  be  spoken,  however,  regarding  its 
use  in  these  cases.  This  symptom  is  usually  observed  in  elderly 
individuals  with  stiffened  arteries  and  degenerated  hearts,  and  as 
the  kidneys  very  commonly  participate  in  this  pathological  pro- 
cess one  should  bear  in  mind  the  possibility  of  these  patients 
being  more  profoundly  affected  by  the  morphine  than  is  desirable 
or  even  safe.  For  this,  as  well  as  other  reasons,  one  should  employ 
the  smallest  dose  that  will  render  the  patient  comfortable.  In 
my  experience  this  is  generally  -1  of  a  grain,  an  amount  which  I 
have  rarely  found  necessary  to  exceed.  In  this  dose  the  remedy 
is  also  a  powerful  cardiac  stimulant,  and  as  such  beneficial  to  this 
class  of  patients. 

III.  BRADYCARDIA 

Bradycardia  and  brachycardia  are  terms  applied  to  an  abnor- 
mally slow  pulse-rate — that  is,  to  one  of  less  than  GO  beats  to  the 
minute.  Allbutt  in  his  system  of  medicine  objects  strenuously 
to  their  employment  on  the  ground  that,  as  slowness  of  the  pulse 
is  but  a  symptom,  they  are  likely  to  mislead  the  student  by  seem- 
ing to  raise  the  symptom  to  the  importance  of  an  independent  dis- 
ease. Nevertheless  the  term  bradycardia  has  come  to  be  so  gen- 
erally used  that  I  have  thought  best  to  follow  the  custom  of  most 
writers  and  give  it  special  consideration.  I  know  by  experience 
that  practitioners  not  only  regard  it  with  apprehension,  but  are 
often  at  a  loss  to  account  for  it,  and  consequently  seek  for  a  state- 
ment of  those  conditions  in  which  it  occurs  and  for  an  explanation 
of  its  significance. 

Slo^vness  of  the  pulse  may  be  cither  physiological  or  pathologi- 
cal. A  normal  pulse-rate  of  less  than  60  is  occasionally  observed, 
but  when  it  is  as  slow  as  30  or  28,  of  which  instances  have  been 
reported,  it  becomes  a  truly  remarkable  ])henomenon.  Napoleon 
Bonaparte  is  often  cited  as  an  instance  of  a  physiologically  slow 
pulse,  having  had  only  40  heart-beats  to  the  minute.  It  has  been 
thought  by  some  that  he  was  a  victim  of  epilepsy,  and  that  his 
bradycardia  was  explicable  on  that  ground.  Physiological  brady- 
cardia is  very  exceptional,  yet  when  encountered  is  not  to  be  re- 
garded as  anywise  likely  to  affect  the  general  health. 


BRADYCARDIA  625 

Osier  states  that  slowness  of  the  pulse  sufficient  to  merit  the 
appellation  of  bradycardia  is  sometimes-  a  family  peculiarity. 
Under  physiological  bradycardia  must  also  be  included  those  in- 
stances sometimes  yet  very  rarely  observed  in  connection  with 
hunger  and  cases  of  transient  slowing  of  the  pulse  said  by  Blot  to 
be  seen  in  about  25  per  cent  of  women  during  the  puerperium. 
In  such  cases  the  rate  may  sink  to  44  or  even  to  34,  Allbutt  has 
noted  bradycardia  in  a  healthy  man  of  forty-nine  given  to  excessive 
sexual  indulgence,  and  has  likewise  seen  it  in  children  as  a  result, 
he  thinks,  of  masturbation.  In  his  own  case  his  pulse-rate  fell  to 
48  and  to  44  in  consequence  of  exhaustion,  for  it  was  restored  to 
its  normal  rate  after  a  refreshing  sleep. 

Romberg,  in  writing  on  diseases  of  the  heart  in  Ebstein's  Prac- 
tice, displays  characteristic  German  exactitude  by  limiting  his 
consideration  of  bradycardia  to  cases  associated  with  cardiac  dis- 
ease. This  appears  to  me  to  be  too  exact,  since  slowness  of  the 
pulse  may  by  the  ignorant  be  thought  to  indicate  heart-disease. 
I  have  decided,  therefore,  to  enumerate  the  diseased  conditions  of 
whatever  kind  which,  according  to  Riegel,  may  be  associated  with 
abnormal  retardation  of  the  pulse.  As  a  basis  for  his  classification 
he  made  a  study  of  1,047  cases  in  which  a  pulse-rate  of  less  than 
60  was  observed.  (1)  Bradycardia  may  occur  during  convales- 
cence from  acute  infectious  diseases,  as  pneumonia,  diphtheria, 
typhoid  fever,  erysipelas,  and  acute  rheumatism.  Sansom  also 
includes  influenza  among  the  acute  disorders  capable  of  producing 
slowness  of  the  pulse,  an  observation  in  which  Allbutt  concurs.  It 
is  believed  that  exhaustion  is  the  cause  in  such  cases.  (2)  Riegel 
observed  this  symptom  in  379  cases  of  disorders  of  the  digestive 
organs,  as  chronic  dysjoepsia,  gastric  ulcer,  cancer,  and  icterus. 
The  occurrence  of  a  slow  pulse  in  cholsemia  is  a  matter  of  frequent 
observation.  Grob  is  also  said  to  have  seen  bradycardia  in  connec- 
tion with  oesophageal  cancer  and  typhlitis.  (3)  The  phenomenon 
under  consideration  is  sometimes  met  with  in  diseases  of  the 
respiratory  organs,  particularly  emphysema  and  (4)  in  diseases  of 
the  heart  and  blood-vessels,  specially  degenerations  of  the  myo- 
cardium depending  on  coronary  sclerosis,  atheroma  of  the  aorta 
(Sansom),  but  is  not  frequent  in  valvular  defects  unassociated 
with  other  alterations  of  rhythm.  In  1  recorded  case  embolism 
of  a  coronary  artery  was  attended  with  a  pulse-rate  of  8  to  the 
41 


626  DISEASES  OF  THE  HEART 

minute.  (5)  Bradycardia  is  occasionally  seen  in  acute  nephritis, 
in  ura3mia,  and  was  seen  in  1  case  of  hematuria  (Sansom).  (6) 
Aside  from  uraemia,  bradycardia  may  be  produced  by  other  poi- 
sons, as  lead,  tobacco  and  coffee,  alcohol  and  digitalis.  (7)  It  is 
sometimes  seen  in  cases  of  diabetes,  chlorosis,  and  anaemia.  (8) 
Apoplexy,  epilepsy,  brain  tumours,  diseases  of  the  medulla  and  of 
the  cervical  portion  of  the  spinal  cord,  paresis,  melancholia,  mania, 
are  all  said  to  sometimes  be  accompanied  by  slowness  of  the  pulse. 
(9)  It  is  sometimes  seen  in  skin  disease,  affections  of  the  geni- 
talia, insolation  and  exhaustion  from  whatever  cause. 

Finally,  with  regard  to  the  pathology  of  bradycardia  it  may 
be  of  interest  to  give  the  following  summary  of  Regnard's  conclu- 
sions presented  in  a  doctoral  thesis  in  July,  1890,  entitled  Etude 
sur  la  pathologic  du  pouls  lent  permanent.  He  is  of  the  opinion 
that  every  chronic  lesion  which  causes  irritation  of  any  portion 
of  the  moderator  apparatus  of  the  heart  may  suffice  to  produce 
permanent  slowness  of  the  pulse  and  give  rise  to  the  aggregate 
of  s^nnptoms.  Such  nervous  irritation  may  have  many  causes, 
as  local  anaemia  through  the  influence  of  atheroma  on  the  periph- 
eral circulation  and  blood-supply  to  the  nerve-centres,  deficient 
blood-supply  to  the  bulbous  portion  of  the  pneumogastric,  tumours 
of  the  meninges  of  the  bulb,  or  in  the  mediastinum  acting  on  the 
vagus,  morbid  excitation  of  the  laryngeal  and  gastric  branches  of 
this  nerve,  but  most  frequently  some  affection  of  the  heart  itself, 
as  fatty  degeneration  or  coronary  sclerosis. 

The  predisposing  conditions  are  stated  to  be  arteriosclerosis, 
whether  syphilitic,  alcoholic,  gouty,  or  rheumatic  in  origin. 

It  is  not  within  the  scope  of  this  work  to  consider  the  signifi- 
cance of  bradycardia  in  other  conditions  than  of  the  circulatory 
apparatus.  In  these  conditions  marked  slowing  of  the  pulse  is 
generally  regarded  as  of  serious  import,  because  it  is  most  com- 
monly observed  in  cases  of  sclerosis  of  the  aorta  or  coronary  arte- 
ries, and  in  such  the  heart-walls  are  likely  to  be  degenerated.  The 
lengthening  of  diastole  incident  to  slow  cardiac  contractions  sub- 
jects the  heart  to  the  possibility  of  diastolic  arrest  and  the  patient 
to  the  possibility,  therefore,  of  sudden  doatli  in  syncope.  Moreover, 
the  heart-muscle  is  extremely  feeble  in  such  cases,  and  hence  it 
may  require  very  little  additional  strain  or  depression  to  bring  it 
to  a  standstill. 


STOKES-ADAMS  DISEASE  627 

I  have  notes  of  an  old  man  witJi  rigid  arteries  and  clironic 
myocarditis  in  whom  for  several  years  prror  to  death  the  pulse- 
rate  was  persistently  abont  28.  In  another  the  heart  Avas  actually 
slow,  but  as  only  every  other  systole  sent  a  blood-wave  to  the  wrist, 
the  pulse-rate  was  in  reality  only  half  as  fast.  It  is  essential, 
therefore,  in  every  instance  of  suspected  bradycardia  that  the 
heart  be  auscultated  to  determine  whether  there  may  not  be  appar- 
ent instead  of  actual  bradycardia. 

IV.    STOKE^ADAMS  DISEASE  {Heart-Block) 

By  this  term  is  designated  a  remarkable  symptom-complex  con- 
sisting in  bradycardia,  vertigo  or  syncope  and  epileptiform  convul- 
sions. Adams  in  1827  and  later  Stokes  were  the  first  to  describe 
cases,  and  hence  this  syndrome  is  called  by  their  names.  For 
many  years  it  was  considered  a  special  disease  and  was  studied 
chiefly  by  English  and  French  clinicians,  but  recently  German 
and  American  physicians  have  contributed  valuable  additions  to 
our  knowledge,  particularly  concerning  the  so-called  bundle  of 
His. 

Heart-hloch  is  a  more  general  term,  since  it  includes  not  only 
the  Stokes-Adams  syndrome  but  all  cases  in  which  there  is  inter- 
ference with  the  conduction  of  stimulus  to  contraction  from  auricle 
to  ventricle  through  the  bundle  of  His.  ISTotwithstanding  previous 
work,  it  may  be  said,  it  is  the  experimental  study  of  Erlanger 
which  has  made  intelligible  the  pathology  of  instances  of  Stokes- 
Adams  disease  that  have  come  to  autopsy  in  the  past  few  years. 

Etiology  and  Pathology. — These  are  no  longer  obscure  and  a 
subject  for  speculation,  as  was  the  case  up  to  1903  when  the  first 
edition  of  this  Avork  appeared.  The  various  theories  once  pro- 
pounded are  now  only  of  historical  interest  and  hence  will  not 
be  described  in  this  place.  Experiments  and  post  mortem  exam- 
inations have  explained  not  alone  the  pathology  of  heart-block,  but 
also  the  morbid  anatomical  changes  underlying  the  Stokes-Adams 
syndrome.  But  before  the  causation  of  this  symptom-complex  can 
be  stated  it  is  advisable  to  describe  briefly  the  system  of  conducting 
fibres  which  are  shown  by  Aschoff  and  Tawara  to  connect  the  right 
auricle  with  the  ventricles. 

This  system  of  fibres  begins  at  the  anterior  edge  of  the  coronary 
vein,  thence  passes  along  the  right  side  of  the  interauricular  sep- 


628  DISEASES  OF  THE  HEART 

turn  below  the  foramen  ovale  to  the  auriciilo-veiitricular  septum, 
where  directly  above  the  point  of  insertion  of  the  median  flap  of 
the  tricuspid  valve  and  before  its  entrance  into  the  connective 
tissue  of  the  septum  it  forms  a  knotlike  mass  of  muscle  fibres. 
From  this  knot  a  band  penetrates  the  fibrous  portion  of  the  septum 
and  running  below  the  nunnbranous  part  of  the  interventricular 
septum  to  its  muscular  portion  here  divides  into  two  main  branches 
which  pass  obliquely  downward  beneath  the  endocardium  one  on 
each  side.  These  two  branches  finally  reaching  the  lower  third  of 
the  ventricles  penetrate  the  pa])illary  muscles,  and  up  to  this  point 
remain  close  underneath  the  endocardium,  through  which  they  usu- 
ally may  be  seen  by  reason  of  their  lighter  color.  Leaving  the 
papillaries  some  of  the  fibres  pass  along  the  course  of  small  tra- 
becular to  the  parietal  wall  of  the  ventricle,  where  running  up 
and  down  beneath  the  endocardial  lining  they  fuse  with  ordinary 
cardiac  muscle  fibres.  Aschoff  further  points  out  that  whereas 
the  right  main  trunk  is  fairly  narrow,  the  left  spreads  out  quickly 
like  a  fan  and  increasing  in  width  as  it  descends  divides  into  two 
broad  but  thin  branches,  of  which  each  passes  to  a  papillary  muscle. 

These  conducting  fibres,  especially  in  the  brownish  hearts  of 
the  old,  but  even  in  the  young,  may  be  discerned  by  the  unaided 
eye  because  of  their  light  yellow  hue.  The  microscope  shows  them 
relatively  poorer  in  sarcoplasm  than  are  ordinary  cardiac  muscle 
fibres,  and  to  hav(;  a  tendency  to  a  reticular  arrangement,  being 
in  this  respect  rather  like  embryonic  muscle  fibres.  This  ap- 
pearance is  most  marked  in  the  auricular  portion  of  the  bundle 
an<l  in  the  knot.  Below  the  knot  the  fibres  are  more  couipact, 
ri<'her  in  sarcoplasm  and  contained  within  a  connnon  sheath.  They 
stain  but  poorly. 

The  function  of  this  conducting  system  luis  been  investigated 
by  physiologists,  notably  Erlanger,  but  space  forbids  more  than 
brief  summary  of  their  results.  Erlanger  by  means  of  a  cleverly 
devised  clamp  was  able  to  compress  and  even  crush  tlie  bundle  of 
His  at  its  auriculo-ventricuhir  junction.  He  found  in  his  experi- 
ments on  dogs  that  conijn-ession  of  the  bundle  caused  slowing  of 
ventricular  contractions  proportionate  to  the  degree  of  interference 
with  the  passage  of  the  excitation  wave  from  the  auricle  to  the 
ventricle.  Slight  degrees  of  compression  produced  partial  heart- 
block  when  two,  three  or  four  auricular  systoles  were  required  tQ 


STOKES-ADAMS  DISEASE  629 

stimulate  the  ventricle  to  contraction.  With  still  greater  compres- 
sion the  ventricular  response  was  still  more  ^interfered  with^  until 
at  length  tlie  tightening  of  the  clamp  caused  complete  heart-block 
or  dissociation  of  auricles  and  ventricles.  When  this  state  was 
reached  the  ventricle  remained  so  long  in  diastole  that  to  prevent 
the  death  of  the  dog  the  inherent  power  of  the  ventricle  to  contract 
had  to  be  aroused  by  tapping. 

From  the  preceding  description  of  thfe  course  and  function 
of  the  conducting  fibres  (the  bundle  of  His)  we  are  in  position 
to  understand  the  etiology  and  symptoms  of  Stokes-Adams  disease. 
In  a  word,  it  is  a  manifestation  of  heart-block  which  when  com- 
plete results  in  the  death  of  the  individual.  Since  Stengel's  case 
was  reported  in  1905  a  number  of  others  have  come  to  autopsy, 
so  that  now  the  following  has  been  ascertained  concerning  the 
pathological  conditions  responsible  for  this  remarkable  syndrome. 

These  cases  have  all  shown  disease  either  of  the  conducting 
fibres  themselves  or  of  the  contigvious  structures  of  such  a  nature 
as  to  interfere  with  the  conduction  of  stimuli  from  auricle  to 
ventricle.  Space  precludes  a  detailed  account  of  these  cases,  but 
the  following  morbid  anatomical  lesions  have  been  discovered. 

In  Stengel's  case  there  was  a  patch  of  atheroma  which  extended 
from  the  base  of  the  anterior  mitral  leaflet  into  the  endocardium 
directly  over  the  bundle  of  His,  and  on  removal  of  the  endocar- 
dium was  seen  to  involve  the  conducting  fibres  at  their  auriculo- 
ventricular  junction.  In  the  case  of  Jellick,  Cooper  and  Ophuels 
there  was  anaemic  necrosis  of  the  muscular  septum  in  the  region  of 
the  bundle  of  His  in  consequence  of  recent  thrombosis  of  its  nutri- 
ent artery.  SchmoU's  case  showed  scar  tissue  in  and  around  the 
bundle  of  His  with  atrophy  of  its  fibres.  Handford,  Gruenbaum, 
Keith,  Miller  and  recently  Ashton,  ISTorris  and  Laveuson  have 
reported  the  discovery  of  gummata  so  located  as  to  involve  the 
system  of  conducting  fibres  in  some  part  of  their  course.  In 
Sendler's  case  there  was  a  cartilaginous  tumor  of  the  interven- 
tricular septum. 

Thus  it  is  seen  that  syphilis  appears  to.  have  a  very  close  con- 
nection with  the  Stokes-Adams  syndrome  and  a  number  of  clinical 
observers  have  noted  their  etiological  relationship.  Finally  heart- 
block  has  been  seen  frequently  in  association  with  degenerative 
changes  of  the  myocardium  and  with  chronic  endocarditis. 


030  DISEASES  OP  THE  HEART 

Symptoms. — The  features  of  this  singiihir  eliiiical  picture  may 
vary  in  intensity  according  as  the  heart-block  is  partial  or  com- 
plete, but  in  order  of  frequency  are  as  follows:  (1)  Bradycardia 
and  other  phenouiena  connected  with  the  circulatory  apparatus; 
(2)  vertigo  or  syncopal  attacks;  (8)  epileptiform  convulsions; 
and  (-i)  disorders  of  respiration.  The  first  three  are  the  most 
common  by  far,  and  in  cases  displaying  all  of  them  it  is  not  always 
possible  to  determine  which  ushers  in  the  series.  It  seems  to  be 
held  generally,  however,  that  the  peculiarity  of  the  heart's  actiim 
soon  to  be  described  is  the  first  to  appear. 

In  most  cases  the  pulse  is  habitually  infrequent  and  usually 
regular,  but  now  and  then  persons  may  be  encountered  who  suffer 
from  periods  of  ])artial  heart-block  and  whose  pulses  meantime 
are  of  normal  or  accelerated  rate.  During  the  attack  the  brady- 
cardia becomes  more  pronounced  so  that  the  pulse  may  fall  to 
twelve,  eight  or  even  five  to  the  minute  as  in  Ilalberton's  case. 
Stengel  noted  in  his  case  a  ventricular  silence  of  2  min.  and  10 
sec.,  Ividd  of  60  sec.  and  Laslett  of  90  sec.  Its  rate  bears  a 
constant  relationship,  however,  to  that  between  attacks.  Thus  a 
pulse  of  '')G,  as  noted  by  His  during  the  intervals,  may  sink  to  18 
during  the  seizure,  proving  that  its  original  rhythm  was  not  dis- 
turbed. In  my  case  reported  on  page  324  irregailarity  in  the 
intervals  between  the  waves  was  noted  and  the  systolic  blood- 
pressure  was  high,  165  mm.  by  Gaertner's  tonometer.  Another 
feature  upon  which  Jaquet  connnents  and  observed  in  my  case  is 
the  obstinate  persistence  of  the  bradycardia  during  the  intervals 
as  well  as  during  the  attacks.  No  amount  of  exercise  and  no 
stimulant  was  able  to  accelerate  the  rate  above  26,  and  yet  strangely 
enough  there  were  times  when  it  rose  apparently  without  cause  to 
normal  or  higher  ami  just  ])rior  to  death  the  nurse  registered  the 
pulse  as  120. 

If  the  heart  is  auscultated  during  an  attack  no  sounds  may 
be  heard  in  the  intervals  between  the  pulse-waves,  but  in  some 
cases  one  or  more  very  feeble  cardiac  tones  are  audible.  This 
peculiarity  lias  been  noted  by  many  observers  and  by  myself,  and 
when  present  may  enable  one  to  make  the  diagnosis  of  heart-block 
without  the  aid  of  an  instruuient.  The  tones  are  not  accompanied 
by  perce])til)le  iui])uls(!  iu  the  heart  region,  and  on  this  account 
Stokes   long  before  the   in\<ution   of  the*  j)olygraph  was  able  to 


STOKES-AbAMS   DISEASE  631 

forecast  correctly  the  fact  proven  instrumcntallj  that  they  are 
due  to  auricular  systoles. 

Another  interesting-  and  singular  phenomenon  first  descriljed 
by  Stokes  is  the  appearance  in  the  internal  jugular  veins  directly 
above  the  clavicles  of  two  or  more  tiny  pulsations  occurring  in  the 
interval  between  ventricular  systoles.  For  many  years  these  feeble 
venous  pulses  were  not  understood,  Stokes  and  others  believing 
them  to  be  auricular  in  origin,  while  Jaquet  and  others  as  stoutly 
maintained  them  due  to  weak  or  abortive  contractions  of  the  ven- 
tricles. In  the  description  of  my  case  already  alluded  to  I  gave 
reasons  for  believing  they  were  ventricular,  but  tracings  by  Mac- 
kenzie's polygraph  in  numerous  instances  since  1903  have  proven 
beyond  question  that  they  are  synchronous  with  auricular  systoles. 
Indeed  it  is  on  the  occurrence  of  these  without  answering  ven- 
tricular contractions  that  reliance  is  placed  for  the  diagnosis  of 
heart-block.  The  number  of  such  venous  pulsations  depends  upon 
the  degTce  of  heart-block.  In  my  case  they  were  generally  two  in 
number,  but  during  the  Stokes-Adams  attacks  reached  as  many  as 
seven. 

If  a  simultaneous  tracing  is  recorded  of  pulsations  in  the 
jugular  and  in  the  carotid  and  such  tracings  are  carefully  meas- 
ured and  interpreted,  they  indicate  plainly  that  these  auricular 
pulsations  or  contractions  do  not  call  forth  answering  systoles  on 
the  part  of  the  ventricles.  In  other  words  there  is  a  loss  of  con- 
ductivity of  the  stimulus  to  contraction  from  the  auricle  to  the 
ventricle,  and  when,  as  in  my  case,  these  auricular  contractions 
number  as  high  as  5,  6,  or  7,  a  condition  of  complete  heart-block 
exists. 

Vertigo  is  experienced  to  a  greater  or  less  degTee  in  all  cases, 
and  annoyed  my  patient  for  over  two  years  before  more  alarming 
symptoms  aj)peared.  The  assumption  of  the  dorsal  decubitus  may 
not  prevent  its  occurrence  or  even  mitigate  its  severity.  That  this 
should  be  so  is  readily  intelligible  when  we  consider  that  the  pro- 
longed diastole  of  the  left  ventricle  must  occasion  some  degree  of 
cerebral  anaemia.  When  this  lack  of  arterial  flow  to  the  brain 
becomes  more  pronounced  it  may  be  declared  by  distinct  faint- 
ing fits. 

Syncope  may  or  may  not  be  experienced,  hut  in  cases  of  com- 
plete heart-block  is  a  prominent  symptom.     The  unconsciousness 


632  DISEASES   OF  THE   HEART 

lasts  only  until  the  next  en^^uing  systole  of  the  ventricle  sends  a 
rush  of  arterial  blood  to  the  brain,  which  rush  may  cause  a  sense 
of  congestion  in  the  head  and  may  be  followed  by  a  dull  headache. 
Accordingly,  the  countenance  is  likely  to  present  a  sharp  contrast 
between  the  ashen  ])ullor  ac('umj)anying  the  syncope  and  the  deep 
flush  produced  by  the  sudden  rush  of  a  more  than  normal  amount 
of  blood  upward  from  the  powerfully  contracting  ventricle. 

The  patient  may  have  no  knowledge  of  what  has  occurred  or, 
as  in  my  case,  he  may  awake  with  a  full  realization  of  the  fact 
that  he  has  fainted.  During  the  time  of  the  syncope  the  attendant 
l)erceives  no  2)ulse  in  any  of  the  arteries  and  may  not  be  able  even 
to  detect  any  heart  sounds.  Consequently,  if  the  intermission  per- 
sists for  a  minute  or  more,  it  is  calculated  to  cause  great  uneasiness 
in  the  minds  of  the  bystanders  lest  in  reality  the  patient  be  dead. 

Mild  epileptiform  convulsions  are  apt.  to  be  shown  during  the 
syncope.  These  may  be  no  more  than  a  twitching  of  tlie  mouth, 
but  are  generally  observed  in  one  or  more  of  the  extremities.  In 
my  patient  the  convulsive  movements  were  confined  to  the  right 
arm  and  the  comers  of  the  mouth.  In  most  instances  there  are 
no  foaming  at  the  lips,  w^ounding  of  the  tongue  or  involuntary 
discharge  of  urine  or  faeces.  Yet  biting  of  the  tongue  ha.^  been 
noted,  and  in  a  case  reported  by  His  there  was  involuntary 
evacuation  of  the  contents  of  the  bladder. 

Huchard,  I  believe,  was  the  first  to  direct  attention  to  the 
association  of  these  epileptoid  convulsions  with  the  bradycardia 
and  vertigo  previously  noted.  In  some  instances  the  clinical  pic- 
ture so  closely  resend)les  an  attack  of  (jrand  tnal  that  it  is  not  at 
all  strange  errors  in  diagnosis  luive  been  made  and  cases  of  Stokes- 
Adams  disease  mistaken  for  genuine  epilepsy. 

Disturbance  of  respiration  has  been  mentioned  as  the  fourth 
symptom  of  this  singular  grouj).  It  may  occur,  but  is  not  at  all 
common,  and  is  said  to  consist  of  ( 'heyne-Stokes  breathing  that 
may  take  place  at  any  period  of  the  attack.  It  W'as  observed  by 
His,  I  believe. 

Finally,  this  symptom-complex  may  take  place  at  long  or  short 
intervals,  but  as  a  rule  not  daily  or  many  times  a  day.  Yet 
])atients  liave  been  known  to  have  frequently  recurring  attacks  for 
an  hour  or,  indeed,  during  the  greater  part  of  a  day.  An  interval 
of  hours,  <]ays,  weeks  or  even  months  may  ensue,  l)ut  when  the 


STOKES-ADAMS  DISEASE  633 

lesion  on  which  depends  the  interference  with  conductivity  is  so 
grave  as  to  lead  to  coni]:)lete  heart-block  the  symptom-free  intervals 
are  not  likely  to  be  so  long.  It  is  readily  intelligible  why  this 
should  be  so  in  cases  of  complete  heart-block  depending  upon 
structural  alterations  in  the  bundle  of  Ilis,  but  why  an  individual 
should  display  the  phenomena  of  Stokes-Adams  disease  at  irregu- 
lar intervals  through  a  period  of  years,  as  in  my  case,  and  then 
die  suddenly  seems  not  quite  clear.  It  is  probable,  however,  that 
other  extraneous  influences  serve  to  depress  the  irritability  of  the 
ventricular  muscle,  thus  rendering  it  less  sensitive  than  ordinary 
to  the  enfeebled  stimuli  from  the  auricles,  or  that  for  the  time 
being  they  still  further  diminish  the  conductivity  of  the  stimulus 
to  contraction  itself.  Upon  such  a  hypothesis  it  is  explicable  that 
the  interference  with  the  passage  of  the  stimulus  from  the  auricle 
or  the  reduction  in  the  irritability  of  the  ventricle  may  reach  such 
a  degree  at  any  time  as  to  lead  to  a  fatal  syncope.  Curiously 
enough  the  young  man  whom  I  had  under  observation  for  so  long 
is  reported  by  his  nurse  to  have  walked  to  his  residence,  seated 
himself  to  read  the  morning  paper,  and  a  few  minutes  thereafter 
to  have  died  suddenly,  although  his  pulse  directly  after  his  return 
to  the  house  was  running  at  120  per  minute. 

In  this  patient  the  influences  which  seemed  to  call  forth  his 
attacks  appeared  to  reside  in  the  intestinal  tract.  This  conclusion 
seemed  warranted  by  the  fact  that  during  the  time  he  was  having 
attacks  his  urine  was  deficient  both  in  quantity  of  water  and  in 
solids,  with  an  indican  percentage  strictly  within  normal  limits. 
Upon  cessation  of  the  attacks  his  urine  improved  in  character  and 
in  particular  the  indican  rose  to  three  to  four  times  the  normal 
amount.  Moreover,  when  he  adopted  a  strict  vegetarian  dietary 
designed  to  correct  his  chronic  constipation  he  enjoyed  many 
months  of  immunity  from  his  symptoms.  That  there  was  a  con- 
dition of  auto-infection  which,  acting  upon  a  diseased  conducting 
system,  in  some  way  evoked  the  seizures  is  in  line  also  with  the 
observation  made  by  Jaquet,  since  in  his  jjatient  many  months 
of  freedom  followed  the  correction  of  constipation  and  indiges- 
tion, while  upon  return  of  these  digestive  disturbances  four  attacks 
supervened,  in  the  fourth  of  which  the  man  died. 

Heart-block  may  develop  at  any  age,  but  inasmuch  as  the 
lesions  likely  to  affect  the  bundle  of  His  somewhere  in  its  course 


634  DISEASES  OF  THE   HEAKT 

are  siicli  as  occur  by  jDreferciice  late  in  life,  the  symptoms  bearing 
the  names  of  Stokes  and  Adams  have  been  observed  mainly  in 
persons  well  on  in  years.  Thns  Adams's  original  case  was  in  a 
man  of  sixty-eight  and  Stokes's  two  were  in  men  of  fifty-six  and 
sixty-eight  respectively.  The  first  instance  coming  to  my  notice 
was  in  an  old  man,  and  as  a  matter  of  fact  this  singular  syndrome 
is  in  the  aggregate  not  very  infrequent  among  the  old. 

For  many  years  the  disease  was  believed  to  be  limited  to  the 
late  period  of  life  when  sclerotic  changes  in  the  vascular  system 
are  common,  which  circumstance  led  to  some  of  the  hypotheses 
advanced  in  explanation  of  its  occurrence.  At  length  His  and 
Jaquet  and  a  few  others  encountered  typical  examples  in  young 
individuals.  This  upset  some  of  the  theories  thought  to  account 
for  it  in  the  aged  and  sclerotic.  Hence  Jaquet  concluded  there 
were  two  groups  of  cases,  one  confined  to  the  old  and  one  to  the 
young.  Now  that  recent  investigations  have  cleared  up  the  pa- 
thology of  this  once  mysterious  group  of  symptoms  we  have  come 
to  realize  that  individuals  at  any  age  may  be  befallen  provided 
their  conducting  system  has  its  integrity  compromised  by  some 
one  of  the  lesions  discovered  in  recent  pathological  investigations. 

Diagnosis. — This  should  present  little  difficulty  when  the  symp- 
toms are  pronounced.  The  conjunction  of  bradycardia,  vertigo 
or  syncope  and  epileptiform  convulsions  occurring  in  paroxysms 
or  attacks  should  suggest  the  malady  to  any  one  familiar  with 
published  descriptions.  If  in  addition  the  patient  is  advanced  in 
age  or  is  found  on  physical  examination  to  possess  a  cardiac 
lesion,  the  real  nature  of  his  attacks  becomes  reasonably  certain 
even  though  he  be  seen  for  the  first  time  during  one  of  his  symp- 
tom-free intervals.  Certainty  of  diagnosis  is  possible,  however, 
only  by  the  recognition  of  the  vascular  and  cardiac  evidences  of 
heart-block. 

Th('s(?  sii>Tis  consist  in  two  or  more  visible  pulsations  of  the 
internal  jugular  veins  without  corresponding  ai)ex-beats  or  carotid 
pulses,  yet  synchronous  with  distant,  feeble  heart  tones.  In  other 
words,  for  every  systole  of  the  ventricle  there  are  two,  three  or 
more  auricular  contractions  whicli  declare  themselves  by  scarcely 
audible  heart  sounds  and  simultaneous  waves  or  ])ulsations  in  the 
jugulars  without  answering  ])ulse-waves  in  the  arteries.  Such  a 
state  of  things  can  exist  only  when  there  is  a  block  to  the  passage 


STOKES-ADAMS   DISEASE  635 

of  stimuli  from  tlic  auricle  to  the  ventricles  and  lionce  the  detec- 
tion of  these  cardio-vascnlar  signs  esta^blishes  the  nature  of  the 
case  beyond  peradventure. 

Stokes-Adams  disease  must  be  differentiated  from  epilepsy  and 
from  functional  disorders  of  the  heart's  action.  It  is  distin- 
guished from  the  former  by  the  absence  of  the  epileptic  cry,  of 
biting  of  the  tongue  and  of  involuntary  evacuation  of  bladder  and 
rectum  and,  if  the  physician  be  so  fortunate  as  to  witness  the 
attack,  by  the  extreme  slowness  of  the  pulse  and  the  cardio-vascular 
signs  of  heart-block. 

Functional  disturbances  of  cardiac  rhythm  may  be  differenti- 
ated in  favorable  cases  by  inspection  of  the  cervical  veins  and 
auscultation  of  the  heart,  but  the  only  precise  method  of  identi- 
fying extra-systoles  on  the  part  of  auricles  or  ventricles  wbich  may 
simulate  partial  heart-block  is  by  resort  to  some  form  of  poly- 
graph, Mackenzie's  or  Hirschfelder's  modification  of  the  Erlanger 
sphygiuomanometer.  By  careful  measurement  of  the  venous  and 
arterial  tracings  thus  obtained  one  can  determine  the  exact  time- 
relation  of  the  pulsations  and  so  ascertain  whether  or  not  a  block- 
ing of  the  contraction-waves  exists. 

Prognosis. — This  is  exceedingly  grave  since  complete  heart- 
block  is  liable  to  cause  death  at  any'  moment.  A  few  cases  have 
been  reported  which  appear  to  have  recovered,  but  since  Stokes- 
Adams  disease  is  generally  due  to  structural  lesions  within  the 
bundle  of  His,  the  probability  of  recovery  is  very  remote.  The 
cases  offering  such  a  possibility  are  those  presenting  a  specific 
history  in  which  the  symptoms  may  be  due  to  gumma  involving 
the  conducting  fibres.  Even  in  such,  however,  the  administration 
of  iodides  is  not  always  capable  of  bringing  about  a  cure.  If  the 
patient  is  old  and  sclerotic  he  will  succumb  to  his  malady  in  all 
likelihood  during  an  attack. 

Treatment  of  this  disease  is  highly  unsatisfactory  because  of 
the  fact  that  with  the  possible  exception  of  syphilitic  disorders 
of  the  heart  we  have  no  means  of  removing  the  cause  under- 
lying the  heart-block.  We  are  restricted,  therefore,  to  a  symp- 
tomatic line  of  therapy,  and  even  this  is  unprofitable  in  most 
instances.  Between  attacks  the  general  health  may  receive  atten- 
tion, and  digestive  disorders,  constipation,  etc.,  should  be  removed. 
The  individual  should  be  warned  against  acts  which  may  over- 


636  DISEASES   OF  THE   HEART 

strain  his  heart  and  should  lead  as  orderly  an  existence,  free  from 
excitement,  as  possible.  Experience  has  proven  that  no  stimulants 
of  any  sort  are  capable  of  terminating  an  attack.  Nevertheless, 
ammonia  or  camphor  may  be  administered,  but  digitalis  and  allied 
drugs  are  distinctly  dangerous.  The  fact  is,  the  symptoms  will 
disappear  or  not  as  the  case  itself  may  determine,  and  hence 
stimulants  may  receive  the  credit  when  no  credit  is  due. 


CHAPTEK    XXV 
ANGINA    PECTORIS 

Definition. — Attacks  of  intense  pain  in  the  region  of  the  heart, 
with  more  or  less  disturbance  of  cardiac  action,  usually  accompa- 
nied by  a  feeling  of  constriction  of  the  chest  and  a  sense  of  im- 
pending death. 

History. — Although  this  form  of  heart-pain  was  not  systematic- 
ally described  until  the  latter  part  of  the  eighteenth  century,  yet  a 
graphic  account  of  his  own  sufferings  from  this  complaint  was 
given  by  Seneca,  and  in  1707  Morgagni  gave  a  clear  description 
of  a  paroxysm  in  a  case  of  aortic  aneurysm.  In  February,  1768, 
Rougnon  addressed  a  letter  to  M.  Lorry  which  contained  the  de- 
scription of  the  death  of  a  certain  Captain  Charles,  who,  from 
the  account  given  by  Rougnon,  appears  to  have  suffered  from  at- 
tacks of  angina  pectoris.  It  was  Heberden,  however,  who  in  July, 
1768,  first  systematically  described  this  formidable  complaint  and 
who  gave  it  the  name  by  which  it  is  now  universally  recognised. 
The  names  of  John  Hunter,  Edward  Jenner,  and  Parry  are  also 
intimately  associated  with  its  early  history.  Hunter  having  expe- 
rienced it  in  his  own  person,  and  having  ultimately  died  in  an 
attack. 

Jenner  in  1799  pointed  out  a  definite  connection  between  scle- 
rosis of  the  coronary  arteries  and  angina  pectoris.  He  is  said  to 
have  refrained  from  publishing  his  views  at  an  earlier  date  out  of 
consideration  for  his  famous  friend,  John  Hunter,  who  during 
his  life  had  held  contrary  opinions  concerning  its  etiology.  Parry 
gave  it  the  name  of  "  syncope  anginosa,"  for,  although  he  recog- 
nised its  connection  with  coronary  disease,  he  considered  the  at- 
tacks due  to  paralysis  of  the  heart. 

From  this  time  forward  the  literature  of  the  profession  teems 
with  contributions  on  the  subject  and  with  divers  theories  con- 

637 


638  DISEASES   OF  THE   HEART 

cerning  its  pathogenesis.  Most  of  the  earlier  writers  attributed 
the  complaint  to  morbid  anatomical  changes  in  the  heart  itself. 
In  181G  Kreysig  definitely  stated  that  it  was  due  to  ischwmia  of 
the  myocardium  in  consequence  of  defective  blood-supply  from 
sclerosis  of  the  coronary  arteries.  In  1821  Reeder  amplified  the 
theory  of  cardiac  ischa-mia  by  asserting  that  this  condition  might 
proceed  not  only  from  ossification  of  the  coronaries,  but  also  from 
any  other  disease — i.  e.,  as  atheroma  of  the  aorta— which  might 
be  capable  of  shutting  off  the  blood-supply  to  the  heart-muscle. 
This  same  theory  was  likewise  espoused  by  Tiedemann  in  1843, 
and  in  1875  Germain  See  described  the  case  of  an  elderly  man 
who  had  suffered  from  anginal  seizures  and  in  whom  after  his 
sudden  death  the  mouths  of  the  coronary  arteries  were  found 
almost  obliterated  by  atheromatous  plaques  situated  on  the  intima 
of  the  aorta.  Throughout  the  balance  of  their  course  the  coro- 
nary vessels  were  healthy.  These  few  instances  are  sufficient  to 
show  in  a  general  way  the  trend  of  opinion  on  the  part  of  the  sup- 
porters of  the  so-called  anatomical  theory. 

In  1834,  says  Iluchard,  the  theory  of  the  purely  nervous  mech- 
anism of  the  attacks  was  formally  announced  by  Gintrac,  although 
its  neuralgic  character  had  been  previously  asserted  by  Baumes  in 
1808,  and  others.  Gintrac  attributed  the  pain  to  irritation  of  the 
fibres  of  the  cardiac  plexus,  and  in  1863  Lancereaux  published  3 
cases  in  which  the  autopsy  revealed  inflammatory  or  other  changes 
of  this  plexus. 

There  has  been  wide  variance  of  opinion  among  French  au- 
thors concerning  the  nerves  implicated.  Thus  Laennec  considered 
it  an  affection  of  the  sympathetic  system  and  called  it  neuralgia 
cordis.  Bouilhnul  regarded  it  as  an  affection  of  the  phrenic 
nerves,  and  Peter,  while  accepting  this  view  as  applicable  to  some 
cases,  also  believed  there  was  a  neuritis  of  the  cardiac  nerves. 
Trousseau  termed  it  an  epileptiform  neuralgia. 

In  Germany  also  the  subject  was  extensively  discussed  and  re- 
ceived a  variety  of  explanations. 

Rond)erg  considers  it  as  a  mere  neuralgia  of  the  cardiac  plexus, 
a  view  not  unlike^  that  of  FricdnM'ch,  who  tliought  it  due  to  hyper- 
a'sthesia  of"  thnt  plexus.  Tlic  ujiuics  ol"  I>aml)erger,  Tnnilx',  Noth- 
tiag(!l,  Landois,  Eulcultcvg,  (luttniaiui,  Leyden,  Kosenbach,  and 
numy  others  are  identified  with  the  literature  of  this  interesting 


ANGi:5rA  PECTORIS  G39 

subject.  Landois,  who  in  1863  subjected  the  question  to  a  critical 
study  from  a  physiological  standj)oint,  divided  angina  pectoris 
into  four  groups,  as  follows:  (1)  Cases  caused  by  disturbance  of 
the  excito-motor  or  accelerator  nerves  of  the  heart;  (2)  those  due 
to  irritation  of  the  cardiac  branches  of  the  vagus;  (3)  cases  aris- 
ing from  reflex  irritation  of  the  abdominal  viscera — "  angina  re- 
flectoria  " ;  (4)  such  as  arise  from  vaso-motor  disturbance  in  vari- 
ous parts  of  the  body — "  angina  vaso-motoria."  Eulenberg  also 
contributed  an  elaborate  article  on  this  subject  in  Ziemssen's  Cy- 
clopaedia of  Medicine,  vol.  xiv. 

Leyden  considers  the  attack  due  to  degenerative  and  inflam- 
matory changes  in  the  heart-muscle  depending  upon  disease  of  the 
coronary  arteries,  which  changes  lead  to  impairment  of  the  heart's 
function. 

According  to  Rosenbach,  some  alteration  in  the  contractions  of 
the  cardiac  muscle  takes  place,  which  alteration  may,  but  does 
not  necessarily,  lead  to  functional  weakness.  In  consequence  of 
this  change,  irritation  is  imparted  to  the  sensory  tract,  and  this 
stimulus  sets  free  the  various  forms  of  pain  and  anxiety  character- 
istic of  stenocardia,  in  accordance  with  irritability  of  the  sensory 
apparatus  and  the  function  of  the  respective  nerves  composing  it. 
Painful  sensations  are  more  or  less  pronounced  according  to 
whether  the  sensory  centres  are  or  are  not  accustomed  to  the  irri- 
tation to  which  they  are  subjected. 

According  to  Rosenbach's  view,  this  true  heart-pain  is  an  indi- 
cation of  the  heart-muscle  being  less  able  than  usual  to  accommo- 
date itself  to  sudden  change  taking  place  in  the  performance  of 
its  work ;  or,  in  other  words,  its  ability  to  respond  to  demands 
from  without  for  a  display  of  extra  effort  is  impaired.  I^ow  and 
then,  also,  obstacles  residing  in  the  heart  itself  and  capable  of  in- 
terfering with  its  perfect  action  may  interrupt  the  performance  of 
its  regular  work  and  in  like  manner  give  rise  to  the  phenomena  of 
angina  pectoris. 

During  the  century  just  ended  many  contributions  to  this  in- 
teresting subject  have  appeared  in  England  and  America,  of 
which  the  most  noteworthy  were  by  Latham,  Gairdner,  and  Osier. 
The  last  mentioned,  in  his  Angina  Pectoris  and  Allied  States, 
deals  with  the  affection  in  a  very  complete  and  entertaining  man- 
ner.    The  most  exhaustive  discussion  of  the  subject,  however,  to 


640  DISEASES  OF  THE   HEART 

vvliich  I  have  had  access  is  that  by  Huchard.  His  historical 
resume  of  the  various  theories  is  complete  and  shows  painstaking 
research.  His  own  view  of  the  pathogenesis  of  this  formidable 
complaint  is  highly  suggestive  and  will  be  stated  in  the  appropri- 
ate place. 

Pathology  and  Etiology. — It  should  be  clearly  understood 
at  the  outset  that  angina  pectoris  is  but  a  symptom  and  not  an 
independent  affection.  It  therefore  can  have  no  morbid  anatom- 
ical characters  peculiar  to  itself.  Its  patljology  is  obscure,  and 
hence  there  have  been,  and  are  still,  various  theories  to  explain 
its  nature  and  mode  of  production. 

It  may  be  stated  in  a  general  way  that  .angina  pectoris  is 
divisible  into  two  forms:  one  incurable  and  likely  to  terminate 
in  death,  the  other  curable  and  not  likely  to  end  fatally.  Some 
authors,  therefore,  following  Walshe's  classification,  speak  of  a 
true  and  a  false  angina.  Osier  makes  this  distinction,  while  Bal- 
four, Gibson,  and  others  consider  such  a  division  irrational  and 
unscientific,  on  the  ground  that  all  pain  is  real,  and  that  there 
can  be  no  such  thing  as  true  pain  and  false  pain.  There  can  be 
no  great  objection  to  these  terms  if  it  is  understood  that  they  are 
employed  for  the  sake  of  convenience,  to  distinguish  grave  cases 
from  those  that  are  not  grave. 

Huchard  also  classifies  cases  of  angina  which  are  purely  neu- 
rotic and  not  likely  to  terminate  fatally  under  the  head  of  pseudo- 
angina,  which  he  makes  include  the  reflex  and  toxic  forms.  In 
certain  cases,  however,  he  believes  that  nicotine  poisoning  is  capa- 
ble of  producing  the  fatal  form  of  angina  pectoris. 

The  confusion  and  obscurity  wliich  so  long  characterized  the 
consideration  of  this  subject,  and  which  indeed  may  be  said  to 
prevail  largely  even  now,  arose  from  the  attempt  to  make  the  same 
pathology  responsible  for  all  cases  of  pain  that  merit  the  term  of 
angina  pectoris.  On  the  other  hand,  the  recognition  of  two  en- 
tirely diverse  groups  renders  the  subject  clear  and  simple,  so  that 
we  are  able  to  get  a  tolerably  definite  notion  of  its  pathology. 

The  angina  which  always  carries  with  it  the  possibility  of  sud- 
den death,  and  which  therefore  may  be  called  true  or  grave,  is  usu- 
ally associated  with,  and  therefore  thought  to  be  dependent  upon, 
structural  disease  of  the  heart.  Various  lesions  have  been  found 
in  fatal  cases,  but  they  are  all  of  such  a  kind  as  to  interfere  with 


ANGINA   PECTORIS  641 

the  blood-supply  to  the  heart-muscle.  Coronary  sclerosis  is  the 
most  frequent,  but  inasmuch  as  all  cases'  of  this  disease  are  not 
attended  with  angina  pectoris,  it  is  evident  that  there  must  be 
something  more  than  mere  sclerosis  of  these  arteries.  According- 
ly it  has  been  determined  that  it  is  not  so  much  the  fact  of  disease 
of  these  vessels  as  it  is  that  this  disease  must  interfere  with  cardiac 
circulation  if  it  is  to  give  rise  to  attacks  of  angina  pectoris. 

Shutting  off  of  the  blood-supply  to  a  limited  portion  of  the 
myocardium — i.  e.,  by  thrombosis  of  terminal  twigs  or  even  of  a 
branch  of  considerable  size — does  not  apparently  always  occasion 
this  pain.  If,  however,  one  main  trunk,  or,  still  more,  if  both 
trunks  are  occluded,  or  if  their  lumen  is  sufficiently  narrowed 
without  being  actually  obstructed,  then  attacks  of  angina  are  very 
likely  to  occur.  Accordingly,  a  condition  which  is  specially  apt 
to  result  in  anginal  seizures  is  narrowing  of  the  mouths  of  the 
coronary  arteries  by  the  sclerotic  process,  as  has  been  repeatedly 
proved  at  the  necropsy  in  cases  of  this  terrible  agony. 

It  is  upon  the  evidence  furnished  by  such  discoveries  that  the 
theory  has  been  reared  of  ischa?mia  of  the  heart-muscle  being  the 
essential  pathological  factor  in  the  causation  of  the  fatal  form 
known  as  true  or  grave  angina  pectoris.  In  this  variety  pain  is 
usually  absent  so  long  as  the  individual  is  at  rest  or  is  not  making 
exertion  that  requires  unwonted  labour  on  the  part  of  the  heart. 
Under  such  conditions  the  circulation  of  blood  within  the  myo- 
cardium is  sufficient  for  its  needs,  but  when  some  emotion  or  extra 
physical  effort  calls  for  unusual  heart-work,  the  narrowed  coronary 
arteries  are  incapable  of  supplying  the  organ  with  an  additional 
volume  of  blood  and  the  ischsemia  is  intensified  for  the  time  being. 
Thereupon  an  attack  of  angina  pectoris  is  evoked.  According  to 
this  hypothesis,  the  nerve-filaments  or  ganglia  with  which  the 
myocardium  is  so  richly  supplied  become  irritated  by  this  depriva- 
tion of  required  blood  and  send  an  impression  through  the  cardiac 
plexus  up  to  the  centre,  which  then  responds  by  discharging  a 
sensation  of  pain  along  certain  nerve-trunks  connected  with  cer- 
tain segments  of  the  spinal  cord.  This  will  again  be  considered  in 
greater  detail. 

The  pain  thus  induced  promptly  causes  a  cessation  of  exertion 
and  consequent  lessening  of  the  heart's  work.  As  the  organ  re- 
sumes its  accustomed  tranquility  its  blood-supply  proves  again 
42 


642  DISEASES  OP  THE  HEART 

sufficient  for  its  needs,  irritation  ceases,  and  with  it  at  last  goes 
the  pain.  Whether  or  not  this  is  the  actual  modus  operandi  of  the 
attack,  the  assumption  that  it  depends  upon  a  diminution  of  the 
blood-supply  seems  borne  ovit  by  the  nature  of  other  cardiac  and 
vascular  lesions  sometimes  discovered  in  fatal  cases  of  angina — 
i.  e.,  aneurysm  and  atheroma  of  the  ascending  aorta,  insufficiency 
of  the  aortic  valves,  and  very  rarely  extreme  degrees  of  aortic  and 
mitral  stenosis.  In  cases  of  angina  that  appear  due  to  aortic  scle- 
rosis the  mouths  of  the  coronary  arteries  are  very  commonly  found 
extremely  reduced  in  size  by  reason  of  calcareous  plaques  on  the 
surface  of  the  intima  or  by  calcareous  thickening  of  the  aortic 
wall,  while  the  coats  of  the  nutrient  arteries. are  also  generally 
invaded  by  the  same  sclerotic  process.  In  cases  of  aneurysm  the 
coronaries  are  narrowed  either  by  the  direct  effect  of  the  aneurysm 
or  by  associated  atheroma.  In  the  diseases  just  mentioned  the 
changes  must  be  of  a  kind  to  obstruct  blood-flow  into  the  coronary 
arteries  if  they  are  to  occasion  the  agonizing  symptom  under  con- 
sideration. 

In  aortic  regurgitation  adequate  blood-pressure  in  the  nutrient 
vessels  is  not  maintained,  and  under  conditions  of  extra  effort  rela- 
tive ischa'mia  of  the  hypertrophied  left  ventricle  is  produced. 
Mitral  and  aortic  stenosis  prevent  the  discharge  of  a  normal  vol- 
ume of  blood  into  the  aorta,  and  consequently  hinder  the  adequate 
flushing  of  the  coronary  arteries.  By  some  authors  the  influence 
of  valvular  defects  in  the  causation  of  angina  is  denied  without 
associated  sclerosis  of  aorta  or  coronaries,  and  certainly  angina 
pectoris  is  exceedingly  rare  in  valvular  disease. 

Nevertheless,  I  have  observed  typical  angina  pectoris  in  one 
case  of  pronounced  aortic  stenosis  that  was,  from  the  history  and 
patient's  age,  presumably  of  rheumatic  origin  and  in  two  instances 
of  aortic  insufficiency.  In  the  first  case  no  autopsy  was  obtained, 
but  in  one  of  the  patients  whose  aortic  incompetence  was  associ- 
ated with  angina  and  whose  case  was  described  in  the  chapter  on 
aortic  regurgitation,  the  pain  was  foinul  to  1)0  clearly  due  to  scle- 
rotic narrowing  of  the  coronaries.  I  am  inclined  to  believe,  there- 
fore, that  aortic  incompetence  of  itself  is  not  so  likely  to  lead  to 
angina  as  is  stenosis. 

Post-mortem  observation  proves  undeniably  that  the  nutrition 
of  the  heart-muscle  may  suffer  seriously  in  cases  of  valve-disease 


ANGINA  PECTORIS  643 

without  associated  coronary  sclerosis,  and  that  such  myocardial 
degeneration  is  particularly  likely  to  be  found  in  long-standing 
and  extreme  stenosis  of  the  aortic  orifice.  This  indicates  that  dur- 
ing a  long  period  of  time  the  demands  on  the  energy  of  the  heart 
outstripped  its  nutrition  owing  to  the  small  supply  of  blood  sent 
through  the  stenosed  orifice  into  the  aorta  and  coronary  system. 

If  in  such  a  state  of  things  the  supply  of  blood  to  the  heart- 
muscle  is  still  further  diminished,  although  but  temporarily,  then 
it  is  possible  for  a  paroxysm  of  angina  pectoris  to  occur.  The  in- 
fluences capable  of  determining  such  a  temporary  increase  of  car- 
diac ischasmia  may  be  vaso-motor  spasm,  affecting  the  coronaries, 
as  suggested  by  Powell,  or  the  continuance  of  undue  physical  exer- 
tion after  such  effort  has  begun  to  overtax  the  heart.  In  extreme 
aortic  stenosis  cardiac  overstrain  is  shown  by  still  greater  feeble- 
ness of  the  pulse,  and  when  such  is  the  case  the  coronaries  are  still 
more  imperfectly  flushed.  There  is  temporarily  a  relative  cardiac 
ischsemia  which  makes  an  attack  of  angina  pectoris  possible.  For- 
tunately such  attacks  are  rare,  yet  on  the  hypothesis  of  cardiac 
ischsemia  as  the  cause  of  angina  the  conditions  favourable  to  its 
production  are  present. 

Finally,  it  should  be  stated  that  the  degenerative  changes  dis- 
covered in  the  myocardium  of  persons  who  have  died  in  a  parox- 
ysm of  angina  pectoris  probably  bear  no  direct  etiological  rela- 
tionship to  the  pain.  Were  it  not  so,  this  formidable  agony  would 
be  far  more  common  than  it  really  is.  Such  degenerations  of  the 
heart-muscle  are  to  be  looked  upon  as  the  result  of  the  pathological 
condition  in  the  coronaries  or  aorta  which  have  led  to  the  angina. 

It  now  remains  to  consider  how  the  morbid  anatomical  condi- 
tions just  mentioned  act  in  the  pathogenesis  of  this  obscure  com- 
plaint. They  are  to  be  regarded  as  predisposing  factors  merely, 
which  to  be  operative  require  some  additional  influence,  since, 
if  such  were  not  the  case,  all  persons  in  whose  heart  such  changes 
are  found  after  death  ought  to  have  suffered  from  angina  pec- 
toris. This  we  know  is  not  the  case.  It  is  this  consideration 
which  has  given  rise  to  the  various  hypotheses  propounded  in 
explanation  of  the  symptom-complex.  The  best  known  of  the  the- 
ories have  been  stated  already  in  the  history  of  the  complaint  and 
do  not  call  for  repetition.  I  would  direct  attention  particularly 
to  Rosenbach's  and  to  that  of  cardiac  ischsemia. 


64:4  DISEASES  OF  THE   HEART 

AVith  reference  to  the  latter,  I  tliink  one  should  also  hear  in 
mind  the  suggestion  of  Sir  Douglas  Powell  that  oftentimes  we 
are  obliged  to  assume  the  possibility  of  relative  cardiac  ischmmia 
if  we  are  to  understand  how  some  cases  originate — i.  e.,  the  condi- 
tions under  which  they  originate,  and  the  beneficial  influence  of 
certain  lines  of  medication.  According  to  this  hypothesis,  vaso- 
motor spasm  may  affect  the  coronary  arteries  and  temporarily 
seriously  diminish  the  flushing  of  the  heart-muscle  with  arterial- 
ized  blood.  The  irritation  thus  evoked  is  declared  by  pain  and 
often  by  disordered  cardiac  action.  AVhen,  upon  administration  of 
vaso-dilators  or  on  cessation  of  arterial  spasm  from  other  influ- 
ences, the  coronaries  become  relaxed,  and  hence  better  flushed, 
irritation  ceases. 

Whatever  is  the  exact  condition,  however,  the  generally  ac- 
cepted view  is  that  there  is  abnornuil  and  excessive  cardiac  irrita- 
tion which  initiates  the  paroxysm.  This  is  Huchard's  view  at  all 
events,  and  herein  he  appears  to  coincide  with  Rosenbach. 

According  to  Iluchard,  the  course  of  vents  in  cases  of  grave 
angina  is  as  follows:  The  heart  itself  is  the  starting-point  of  the 
attack.  From  here  the  stimulus  ascends  by  way  of  the  sensory 
centres  and  finally  reaches  the  medulla.  Thence  it  is  reflected  along 
the  intercostal  nerves  and  brachial  plexus  as  a  manifestation  of 
pain.  The  stimulus  next  reaches  the  vagus  centre,  and  from  here 
an  inhibitory  impulse  is  sent  down  to  the  heart,  the  original  start- 
ing-place, and  declares  itself  by  slowed,  and  it  may  be  intermittent 
action  of  the  heart. 

Such  an  inhibitory  action  explains  the  sense  of  constriction 
and  of  impending  death,  as  well  as  tlie  dilatation  of  the  cardiac 
cavities  sometimes  noted. 

In  pseudo-angina,  on  the  contrary,  the  point  of  departure  of 
the  irritation  is  an  intercostal  nerve  or  some  other  peripheral  or 
visceral  nerve,  whence,  as  in  true  angina,  it  also  passes  to  the 
medulla.  From  there  an  impulse  is  sent  out  not  along  intercostal 
nerves  and  brachial  plexus,  but  is  passed  down  along  the  vagus  or 
accelerator  nerves  of  the  heart  to  this  organ.  According  to  the 
route  thus  selected,  the  action  of  the  heart  becomes  either  rapid  or 
slow  and  otherwise  disordered. 

In  these  two  forms,  therefore,  the  original  source  of  irritation 
is  entirely  different  and  the  circuit  is  traversed  in  a  contrary  di- 


ANGK^A  l^ECTORIS  645 

rection.  To  my  mind  this  is  a  highly  satisfactory  explanation  of 
the  differences  in  their  clinical  phenomena.  It  likewise  proves 
seryiceable  in  making  up  diagnosis  and  prognosis  and  in  deciding 
on  the  mode  of  management. 

Leaving  now  the  pathology  of  angina  pectoris,  which,  however 
much  we  may  speculate  upon  it,  is  undeniably  obscure,  we  come 
to  the  consideration  of  the  remaining  predisposing  causes  as  well 
as  the  influences  which  directly  excite  an  attack. 

Aside  from  the  anatomical  conditions  already  considered,  we 
are  at  once  impressed  by  the  important  part  played  by  age.  An- 
gina pectoris  of  coronary  origin  is  emphatically  a  complaint  of 
individuals  who  have  passed  middle  age  and  have  entered  their 
sixth  or  seventh  decade.  This  is  an  age  in  which  the  effects  of 
arteriosclerosis  usually  declare  themselves,  and  yet  angina  of  this 
origin  is  sometimes  observed  before  the  fiftieth  or  even  the  fortieth 
year.  One  or  two  instances  are  on  record  of  its  occurrence  in  chil- 
dren. ISTevertheless  such  facts  do  not  invalidate  the  correctness  of 
the  statements  made  concerning  the  importance  of  age. 

Males  are  much  more  frequently  affected  than  are  females,  and 
of  men  who  are  befallen  it  is  a  noteworthy  fact  that  it  is  espe- 
cially the  well-to-do  and  well-fed.  Regarding  the  influence  of  sex, 
Osier  states  that  out  of  his  40  cases  but  3  occurred  in  women.  I 
have  notes  of  32  cases,  and  of  these,  7  were  in  the  female  sex. 
Of  '2  that  came  to  autopsy,  1  was  a  woman  of  sixty-six  with  aortic 
and  mitral  stenosis,  with  sclerosis  of  the  aorta  and  coronaries ; 
while  in  the  other,  as  already  stated,  there  was  coronary  obstruc- 
tion and  aortic  regurgitation,  both  of  sclerotic  origin.  Of  the  re- 
maining 5  cases,  1  was  in  an  aged  woman  presenting  well-marked 
signs  of  arteriosclerosis,  a  hypertrophied  left  ventricle,  and  a 
harsh  systolic  basic  bruit.  Another  was  a  comparatively  young 
female  with  aortic  regurgitation  of  uncertain  origin,  but  whose 
questionable  habits  always  made  me  suspicious  of  the  likelihood 
of  syphilitic  infection.  The  third  was  in  the  lady  of  forty-four 
with  signs  of  pure  aortic  stenosis  whose  case  has  been  already  de- 
scribed in  the  chapter  on  Aortic  Stenosis,  and  will  be  again 
alluded  to  in  this.  The  fourth  was  in  a  woman  of  fifty  with  aortic 
regurgitation,  due  probably  to  arteriosclerosis,  to  judge  from  her 
history  and  the  arterial  thickening.  The  fifth  case  was  that  of  a 
woman  of  fifty-six  who  was  corpulent  and  had  thickened  arteries 


G46  DISEASES  OF   THE   HEART 

with  a  greatly  hypertropliied  and  dilated  heart.  As  regards  this 
striking  discrepancy  between  the  two  sexes,  it  may  be  stated  that 
the  greater  prevalence  of  angina  pectoris  among  elderly  men  is  to 
be  referred  not  so  much  to  sex  per  se  as  to  those  conditions  which 
are  responsible  for  the  greater  frequency  of  arteriosclerosis  in  the 
male  sex. 

Heredity  is  also  a  predisposing  factor,  what  was  said  under 
this  head  concerning  coronary  sclerosis  and  myocardial  degenera- 
tion being  also  applicable  to  the  symptom  now  considered.  In- 
stances are  on  record  of  this  formidable  complaint  having  been 
passed  down  through  three  generations.  It  is  not  at  all  uncom- 
mon for  both  father  and  son  to  suffer  or  eveii  die  from  angina 
pectoris.  The  most  notable  instances  of  the  kind  occurred  in  the 
persons  of  Thomas  Arnold,  of  Kugby,  and  his  equally  well-known 
son,  Matthew  Arnold. 

Gout  predisposes  to  arteriosclerosis,  and  therefore  to  angina 
pectoris.  Syphilis,  alcohol,  and,  according  to  Huchard,  tobacco, 
are  also  predisposing  causes.  The  last  named  may,  however,  be  an 
exciting  cause. 

The  exciting  causes  of  true,  or  coronary  angina,  as  Huchard 
calls  it,  are  conditions  that  suddenly  raise  blood-pressure  in  the 
aortic  system,  or,  according  to  the  theory  of  cardiac  ischamiia,  re- 
quire more  work  of  the  heart  than  it  can  perform  in  consequence 
of  its  diminished  blood-supply.  Foremost  among  these  is  muscu- 
lar effort.  The  patient  may  have  had  no  premonition  of  the  mal- 
ady, when,  one  day,  perchance  immediately  after  breakfast,  he 
starts  out  for  a  walk  and  is  arrested  by  an  indescribable  attack 
of  praecordial  pain.  In  other  instances  the  first  paroxysm  is  expe- 
rienced upon  the  patient  attempting  to  hurry  to  reach  a  car,  or 
the  like,  and  thereafter  is  repeated  whenever  he  quickens  his  foot- 
steps beyond  his  usual  pace.  Atmospheric  conditions  undoubtedly 
intensify  the  influence  of  exertion,  for  on  a  day  when  the  wind  is 
easterly  and  raw  these  patients  find  themselves  imable  to  walk 
at  even  their  accustomed  gait ;  while  in  warm  weather  and  on 
still  days,  or  here  in  Chicago,  even  in  the  depth  of  winter 
when  the  air  is  dry  and  cold  and  the  sun  bright,  these  patients 
frequently  find  themselves  able  to  get  about  with  comparative 
comfort. 

I  have  known  patients  who  could  walk  with  ease  when  the 


ANGINA  PECTORIS  647 

stomach  was  empty,  yet  who  invariably  experienced  pain,  of 
greater  or  less  severity,  whenever  attempting  to  walk  soon  after 
breakfast.  This  is  undoubtedly  to  be  explained  by  the  augmenta- 
tion of  arterial  tension,  produced  by  the  presence  of  food  in  the 
stomach.  Nevertheless  the  rise  of  blood-pressure  thus  occasioned 
is  of  itself  not  sufficient  to  evoke  an  attack,  since  it  requires  in 
addition  physical  exertion. 

Emotional  states,  as  anger,  worry,  or  excitement  from  what- 
ever cause,  which  accelerate  and  intensify  cardiac  action,  are  also 
capable  of  evoking  an  attack  of  angina  pectoris.  This  was  illus- 
trated in  the  historic  case  of  John  Hunter,  who  was  wont  to  say 
that  "  his  life  was  in  the  hands  of  any  rascal  who  chose  to  annoy 
or  tease  him."  As  a  matter  of  fact.  Hunter  died  during  a  parox- 
ysm brought  on  by  a  fit  of  silent  rage  in  consequence  of  having 
been  flatly  contradicted  at  a  meeting  of  the  Board  of  Governors  of 
St.  George's  Hospital,  October  16,  1793.  His  coronary  arteries 
were  found  ossified  and  the  aorta  dilated.  I  knew  a  gentleman  of 
this  city,  a  great  sufferer  from  ferocious  attacks  of  angina  for 
many  years,  who  frequently  declared  that  nothing  was  so  bad  for 
him  as  a  fit  of  temper. 

It  is  very  remarkable  how  diverse  are  the  effects  of  exertion  in 
different  persons,  or  in  the  same  individual  at  different  times.  I 
recall  the  instance  of  a  gentleman  of  fifty-two,  who,  by  the  way, 
had  been  an  inveterate  smoker  of  strong  Havana  cigars,  and  who 
could  not  walk  out  of  an  evening  without  suffering  from  his  an- 
gina. Yet  on  one  occasion  he  assisted  in  carrying  a  loaded  book- 
case up  a  flight  of  stairs  without  experiencing  the  slightest  pain. 
This  patient  ul'timately  died  suddenly.  I  have  another  gentleman 
under  occasional  observation  who  invariably  experiences  more  or 
less  pain  of  a  true  anginal  character  the  first  thing  in  the  morning 
when  he  goes  into  the  bath-room  to  dress.  The  taking  of  a  cool 
bath  is  almost  sure  to  evoke  one  of  his  seizures.  Excitement  and 
exertion  combined  are  particularly  apt  to  call  forth  an  attack. 
For  this  reason  coitus  is  especially  injiirious  to  some  of  these  pa- 
tients. The  influence  of  cold  in  determining  a  paroxysm  has  been 
referred  to,  and  is  shoAvn  by  the  inability  of  patients  to  face  a 
cold  wind,  particularly  when  damp  as  well  as  cold,  and  by  the 
effect  of  a  cold  bath. 

Distention  of  the  abdominal  viscera  by  flatus  and  the  taking 


648  DISEASES  OF  THE  HEART 

of  a  full  meal  are  enumerated  among  the  exciting  causes  by  some 
authors,  but  in  my  experience  these  have  been  operative  only  in 
connection  with  other  determining  factors,  as  exertion.  Tobacco 
is  counted  by  Huchard  as  both  an  exciting  and  a  predisposing 
cause,  and  he  narrates  instances  of  individuals  who  had  abandoned 
smoking  because  of  the  attacks  of  angina  it  induced,  and  who  upon 
returning  to  their  former  habit  again  found  it  promptly  followed 
by  the  same  unpleasant  effect, 

Gibson  likewise  speaks  of  tea  and  coffee  in  this  connection,  say- 
ing they  also  claim  their  victims.  Regarding  the  angina  due  to 
tobacco,  Huchard  recognises  three  forms:  (1)  Functional  or  rela- 
tively benign  form,  resulting  from  spasm  of  the  coronary  arteries, 
without  disease  of  the  myocardium,  and  which  is  the  "  Angina 
spasmo-tabagique,"  and  which  is  recovered  from  by  giving  up  the 
use  of  tobacco.  (2)  An  organic  angina  of  a  grave  character,  re- 
sulting from  coronary  sclerosis  and  which  is  not  recovered  from  by 
the  abandonment  of  the  tobacco  habit.  This  is  the  "  Angina 
sclero-tabagique."  (3)  The  form  most  benign  of  all  results  from 
digestive  troubles  produced  by  the  tobacco  habit  (gastralgia,  dila- 
tation of  the  stomach,  and  insensibility  of  the  mucous  membrane). 
This  is  the  "  Angina  gastro-tabagique."  Strictly  speaking,  these 
all,  with  the  possible  exceptions  of  the  second  form,  belong  to  the 
pseudo-angina. 

In  the  group  of  cases  known  as  false  angina,  and  which,  ac- 
cording to  Huchard,  belong  to  the  peripheral  or  visceral  neuralgias, 
and  which  will  be  considered  in  connection  with  cardiac  neuroses, 
the  exciting  causes  are  not  always  easy  of  recognition,  yet,  as 
stated  emphatically  by  Huchard,  are  never  due  to  effort.  Herein, 
therefore,  lies  the  great  distinction  between  true  and  false  an- 
gina. Occasionally  in  true  angina,  the  paroxysms  occur  at  night, 
arousing  the  patient  from  sleep,  but,  according  to  Huchard,  this 
does  not  invalidate  the  statement  that  coronary  angina  is  evoked 
by  effort,  nor  arc  these  cases  to  be  classed  as  pseudo,  because  com- 
ing on  at  night. 

Their  advent  during  sloo])  is  referable  to  some  condition  which 
augments  blood-pressure  and  acts  in  the  same  manner  as  does 
effort  made  by  these  individuals.  Some  of  these  conditions  may 
be  flatulent  distention  of  the  bowels,  coldness  of  the  air  in  the 
sleeping  apartment,   an   uncomfortable  position   during  sleep,   or 


ANGIl^A  PECTORIS  649 

the  recumbent  posture  itself,  which  is  known  to  augment  blood- 
pressure  (llucliard). 

Clinical  History  and  Features  of  an  Attack. — The  sufferer  from 
angina  of  coronary  disease  is  most  often  an  elderly  man  of  about 
sixty  years  of  age  who  has  been  engaged  in  mercantile,  profes- 
sional, or  literary  pursuits  rather  than  in  manual  labour,  and  who 
often  presents  the  appearance  of  well-preserved  health.  He  not 
infrequently  states  that  prior  to  his  first  attack  of  angina  he  never 
had  any  symptoms  that  made  him  think  his  heart  was  affected, 
and  that  were  it  not  for  this  symptom  he  would  still  think  his 
heart  as  sound  as  ever. 

Questioned  concerning  the  symptoms  for  which  he  consults  the 
physician,  he  says  he  has  a  pain  in  the  front  of  the  chest,  which 
he  locates  at  the  upper  and  middle  portion,  frequently  putting  his 
hand  over  the  manubrium  sterni.  He  describes  this  pain  as 
coming  on  suddenly,  usually  during  a  walk,  and  becoming  so 
intense  as  to  compel  him  to  stand  still  until  it  goes  away,  which 
it  usually  does  in  a  few  moments.  Further  inquiry  brings  out 
the  fact  that  associated  with  the  pain  is  a  feeling  of  oppression 
or  weight  on  the  chest,  and  in  some  cases  a  sense  of  impending 
death.  The  essential  features  of  an  attack,  therefore,  or  the  char- 
acteristic triad  of  symptoms,  as  it  may  be  called,  are  (1)  a  subster- 
nal pain,  that  is  usually  so  severe  as  to  be  an  indescribable  agony, 
(2)  a  sense  of  great  constriction  of  the  chest,  a  feeling  as  if  this 
were  being  crushed  or  squeezed  together,  and  (3)  a  sense  of  speedy 
or  impending  dissolution. 

The  duration  of  a  paroxysm  is  not  long,  generally  not  more 
than  a  few  minutes,  probably  because  the  violence  of  the  agony 
necessitates  a  cessation  of  the  effort  occasioning  it,  and  with  the 
removal  of  its  exciting  cause  the  attack  subsides.  Occasionally  it 
persists  for  twenty  minutes  or  more,  and  when  it  occurs  in  the 
middle  of  the  night  it  is  apt  to  last  longer  than  do  day  attacks. 
Thus  it  is  seen  that  the  pain  may  come  on  either  by  day  or  by 
night,  but  as  a  rule  and  particularly  in  mild  cases  it  is  more 
likely  to  manifest  itself  during  the  waking  hours  and  when  the 
patient  is  exposed  to  some  obviously  exciting  cause.  I^octurnal 
seizures  are  apt  to  be  more  severe  as  well  as  of  greater  duration, 
because,  according  to-Huchard,  the  rise  of  blood-pressure  incident 
to  the  recumbent  posture  does  not  subside  quickly  even  after  the 


650  DISEASES  OP  THE  HEART 

patient  leaves  his  bed,  whereas  that  due  to  effort  or  emotion  yields 
promptly  to  the  removal  of  the  cause. 

The  first  seizure  has  been  known  to  prove  fatal,  and  on  the 
other  hand  attacks  have  recurred  at  varying  intervals  for  five, 
ten,  fifteen,  and  even  twenty-five  years.  A  single  sharp  paroxysm 
has  been  followed  by  years  of  immimity,  and  in  other  instances, 
after  having  been  absent  for  a  long  period,  the  malady  has  then 
assumed  a  frequently  recurring  type.  Huchard  speaks  of  the 
paroxj^sms  as  sometimes  occurring  with  such  frequency  as  to  over- 
lap each  other,  and  thus  become  practically  continuous  with  only 
remissions  in  severity,  a  condition  which  he  terms  I'etat  de  mal 
angineux.  Some  patients  are  aware  so  soon  as  they  arise  in  the 
morning  that  they  are  going  to  have  a  "  bad  day,"  as  they  say,  or 
that  they  will  have  to  be  more  than  usually  cautious  lest  they  pre- 
cipitate an  attack.  As  a  rule,  however,  anginal  seizures  come  on 
abruptly  without  warning  and  with  such  agonizing  intensity  that 
the  sufferer  is  compelled  to  stop  in  his  tracks  and  remain  standing, 
scarcely  daring  to  stir  or  breathe  lest  he  intensify  his  pain  beyond 
all  possibility  of  endurance. 

At  other  times  he  leans  against  a  tree  or  wall  for  support,  or 
he  stands  in  some  peculiar  attitude  which  experience  has  taught 
him  will  somewhat  mitigate  the  severity  of  the  pain.  He  may 
lean  forward  or  bend  backward,  let  his  arms  hang  motionless  at 
his  side  or  stretch  them  above  his  head  in  an  effort  to  fix  the 
pectoral  muscles  so  as  to  thereby  increase  the  expansion  of  his 
chest,  which  seems  to  him  to  be  compressed  and  too  small  for  its 
contents.  But  whatever  his  attitude,  it  is,  according  to  Huchard, 
always  an  upright  rather  than  a  recumbent  position,  which  latter, 
by  augmenting  arterial  tension,  increases  the  severity  of  the  attack. 

Most  happily  for  the  patient  the  angina  usually  departs  as 
quickly  as  it  comes,  and  unless  the  attack  has  been  one  of  un- 
usual length  or  severity  tlie  victim  feels  as  well  immediately  after 
as  he  did  before  the  seizure.  He  is  generally  able  to  resume  his 
walk,  although  perhaps  rather  more  cautiously  than  before.  Such 
is  the  history  of  a  comparatively  mild  angina  pectoris,  but  in  some 
sad  cases  thg  attacks  grow  more  fro(picnt  and  more  agonizing  until 
at  length  the  patient  is  not  al)le  to  move  in  bed  or  engage  in  con- 
versation witliout  frightful  suffering,  iiud  life  becomes  a  miserable 
existence. 


ANGINA  PECTORIS  651 

It  now  becomes  necessary  to  consider  the  features  of  anginal 
attacks  in  detail.  It  has  been  stated  that  the  pain  is  subster- 
nal; that  is,  that  its  seat  of  maximum  intensity  or  its  point  of 
departure  is  beneath  the  upper  or  middle  third  of  the  breast- 
bone. It  is  for  this  reason  that  Baumes  applied  to  the  complaint 
the  name  of  sternalgia.  The  pain  may  remain  centred  beneath 
the  sternum,  but  in  most  instances  it  radiates  into  the  side 
of  the  thorax  and  along  the  course  of  the  brachial  plexus  into 
the  left  shoulder  or  down  the  corresponding  arm  to  the  elbow 
or  still  farther,  as  far  as  the  wrist,  or  even  into  the  two  fingers 
supplied  by  the  ulnar  nerve.  In  some  cases  the  pain  takes 
origin  in  the  region  of  the  apex-beat  or  epigastrium,  or,  as  in 
the  case  of  one  of  my  patients,  just  above  the  ensiform  appen- 
dix, whence  it  shoots  into  the  left  shoulder  and  down  the 
left  arm. 

In  rare  instances  the  attack  starts  in  the  arm,  at  the  wrist  or 
elbow,  and  thence  passes  into  the  chest  to  the  region  of  the  heart. 
In  one  of  Trousseau's  patients  the  paroxysm  began  in  the  back 
of  the  neck,  and  then  darted  forward  into  the  tongue  and  front 
of  the  thorax.  Very  exceptionally  the  pain  may  take  origin  in 
the  left  interscapular  region  or  at  the  adjacent  dorsal  spines.  But 
whatever  is  its  point  of  departure  the  anguish  radiates  more  or 
less  widely  throughout  the  chest,  flashing  from  the  cardiac  area 
into  the  left,  sometimes  the  right  arm,  and  in  some  cases  into  both 
arms,  or  upward  into  the  side  of  the  neck  or  the  occiput,  or, 
instead,  downward  into  the  left  half  of  the  abdomen,  and  now  and 
then  even  to  the  thigh.  These  latter  lines  of  radiation  are,  how- 
ever, very  uncommon  as  compared  with  its  course  into  the  left 
shoulder  and  arm. 

Very  diverse  terms  are  employed  by  patients  in  attempts  to 
describe  their  agony.  It  is  spoken  of  as  crushing,  grinding,  tear- 
ing, cutting,  burning,  scalding,  or,  in  want  of  appropriate  adjec- 
tives, as  indescribable,  frightful,  and  the  like.  One  of  my  pa- 
tients, a  lady  with  extreme  aortic  stenosis,  depicted  her  anguish  as 
"  a  feeling  as  if  my  chest  were  being  crushed  beneath  the  wheels 
of  a  passing  train." 

The  sensation  of  pain  is  sometimes  lost  in  the  terrible  distress 
occasioned  by  the  sensation  of  the  chest  being  squeezed  in  a  vise, 
or  of   the   walls   being   forced  together   from   before   backward. 


652  DISEASES  OP  THE  HEART 

Balfour  describes  it  as  if  the  heart  were  being  "  grasped  by  a 
mailed  hand." 

Then,  as  if  this  were  not  enough,  the  sensation  of  impending 
death  is  added,  to  complete  this  awful  suffering.  The  lady  just 
mentioned,  said  in  reply  to  a  query  upon  this  point :  ''  Oh,  yes !  of 
course  I  feel  as  though  I  were  going  to  die,  but  I  have  learned 
by  experience  that  I  do  not  die,  and  therefore  I  no  longer  speak 
about  it.  I  always  used  to  declare  that  I  knew  I  was  going  to 
die."  Nearly  all  sufferers  from  severe  angina  pectoris  agree  in 
the  assertion  that  no  other  pain  can  compare  with  the  awfulness 
of  its  agony,  and  if  it  were  not  happily  of  short  duration,  life 
could  not  endure. 

The  physician  is  not  often  a  witness  of  the  terrible  agony,  the 
attack  being  over  before  he  arrives,  or  his  attention  is  so  occupied 
in  efforts  for  the  patient's  relief  that  he  cannot  note  the  several 
features.  Nevertheless,  from  such  observations  as  have  been  re- 
corded, we  possess  certain  facts  concerning  objective  symptoms. 
The  face  is  expressive  of  unspeakable  agony ;  it  is  anxious  and 
usually  pale,  and  bedewed  with  perspiration,  but  it  may  be  con- 
gested. The  patient  is  usually  motionless  during  the  height  of  the 
Ijaroxysm,  yet  it  may  be  ushered  in  and  terminated  by  restlessness. 
The  extremities  are  usually  cold,  and  the  pulse  is  variable.  It  is 
sometimes  stated  to  be  unchanged,  but  is  for  the  most  part  small 
and  tense. 

It  may  be  regular  or  irregular  and,  if  accelerated  in  the  be- 
ginning, is  likely  to  become  slower  than  normal  before  the  cessa- 
tion of  the  pain.  The  size  and  rate  of  the  pulse  have  given  rise 
to  much  discussion,  but  the  consensus  of  opinion  seems  to  be  that 
it  is  small,  sharing  in  the  condition  of  spasm,  and  that  its  rate  is 
slow,  indicating  vagus  stimulation.  The  heart  sounds  are  usually 
clear,  but  feeble,  although  in  some  instances  a  systolic  apex-mur- 
mur has  been  audible. 

As  already  stated,  the  seizure  usually  subsides  suddenly,  leav- 
ing TKithiiig  more  than  a  feeling  of  weakness  behind.  The  pain  in 
th(!  uj)p('r  extremities  may  be  accom]>anied  but  is  more  often 
fcjllowed  by  a  feeling  of  numbness,  even  by  transient  paresis.  The 
lady  to  whom  reference  has  been  repeatedly  made,  said  her  left 
arm  was  always  helpless  after  cessation  of  the  suffering. 

In  the  case  of  my  aged  female  patient,  already  mentioned  as 


ANGINA  PECTORIS  653 

having  arteriosclerosis,  the  face  was  flushed  during  the  attack, 
and  the  cessation  of  pain  was  followed  by  vomiting.  I  have  stated 
that  i)atients  remain  motionless  during  the  paroxysms,  yet  I  have 
known  two  instances,  both  men,  who  thought  they  obtained  some 
relief  by  walking  gently  about  the  room  while  the  pain  was  on. 
One  of  them  was  a  well-known  attorney,  in  whom  the  necropsy 
verified  the  diagnosis  of  coronary  sclerosis  and  fatty  degen- 
eration of  the  left  ventricle.  In  the  other  case  the  age  of  the 
patient,  the  thickened  peripheral  arteries,  and  the  history  of  the 
attacks,  left  no  doubt  as  to  the  nature  of  his  angina.  Douglas 
Powell  states  that  when  relief  is  produced  by  quiet  walking  it  has 
seemed  to  him  to  indicate  a  fairly  sound  state  of  the  heart-muscle. 
This  may  be  so  in  some  but  not  all  cases.  Mr.  H.,  the  attorney, 
was  found  to  have  extensive  myocardial  degeneration,  and  hence 
some  other  exjDlanation  is  needed  in  his  case.  In  my  other  pa- 
tient, the  gentleman  was  not  only  able  to  endure  without  pain 
certain  gymnastic  and  breathing  exercises  which  produced  great 
perspiration,  but  he  declared  that  he  felt  better  for  them.  That 
they  did  not  call  forth  his  suffering  the  same  as  did  walking 
against  a  wind,  may  have  been  due  to  the  lowering  of  arterial  ten- 
sion which  they  induced. 

The  extremely  variable  course  of  the  malady  and  its  not  in- 
frequent termination  in  death  during  an  attack  are  also  note- 
worthy features.  An  historic  instance  is  that  of  the  Rev.  Dr. 
Chalmers,  who  is  thought  to  have  died  during  a  paroxysm  of 
angina,  since  he  was  found  dead  in  his  bed  with  a  bowl  beside 
him  into  which  he  had  emptied  the  contents  of  his  stomach.  I 
knew  a  similar  instance  of  an  old  gentleman  who,  after  having 
suffered  attacks  of  angina  pectoris  for  twenty  years,  was  found 
lifeless  in  his  bed  in  a  hotel  with  a  wash-bowl  resting  on  the  bed  in 
front  of  him  and  containing  vomited  matter.  I  knew  of  another 
elderly  gentleman  who,  while  in  attendance  upon  a  lawn  fete,  was 
seized  with  a  paroxysm  of  prsecordial  pain,  vomited,  and  imme- 
diately died  before  assistance  could  reach  him.  So  far  as  could 
be  ascertained,  it  was  his  first  and  only  attack. 

Before  leaving  this  subject,  it  should  be  mentioned  that  Gaird- 
ner  has  described  what  he  calls  angina  sine  dolore.  What  he 
means  by  the  term  is  best  described  in  his  own  words :  "  Apart 
from  what  has  been  variously  termed  cardiac  asthma,  dyspnoea, 


654  DISEASES  OF  THE  HEART 

or  orthopnoea,  which  in  many  cases  receives  its  clear  explanation 
from  the  associated  states,  either  of  the  pulmonary  circulation 
or  of  the  lungs,  bronchi,  and  pleura^,  as  disclosed  by  physical 
signs,  there  is  often  an  element  of  subjective  abnormal  sensation 
present  in  cardiac  diseases,  which,  when  it  is  not  localized  through 
the  coincidence  of  pain,  is  a  specially  indefinable  and  indescrib- 
able sensation,  almost  always  felt  to  be  such  by  the  patient  him- 
self. I  make  this  remark  deliberately,  as  the  result  of  experience, 
and  well  knowing  it  is  liable  to  be  brought  into  question  in  par- 
ticular instances — that,  in  fact,  a  large  part  of  what  has  been  de- 
scribed under  the  titles  given  at  the  commencement  of  this  para- 
graph has  been  inextricably  confounded  by  systematic  writers 
with  the  sensation,  or  group  of  sensations,  to  which  I  refer. 

To  this  group  of  sensations,  when  not  distinctly  accompanied 
by  local  pain,  I  have,  in  various  instances,  given  the  name  of 
angina  sine  dolore,  recognising  thereby  what  I  believe  to  be  its 
true  diagnostic  and  pathological  significance,  and  its  alliance  with 
the  painful  angina  of  Heberden ;  the  pain  in  which,  however,  as 
we  have  already  seen,  is  an  exceedingly  variable  element,  both  in 
degree  and  in  kind." 

Diagnosis. — Two  questions  present  themselves  for  answer 
in  the  diagnosis  of  this  formidable  complaint:  First,  is  the  attack 
of  pain  angina  pectoris  ?  and  second,  what  is  the  pathological  con- 
dition underlying  the  attack  ?  In  other  words,  is  the  paroxysm 
to  be  classed  as  coronary  angina  ?  or  is  it  a  disorder  of  the  nervous 
system  independent  of  any  cardiac  or  vascular  disease  ?  In  at- 
tempting to  answer  the  first  query,  one  should  keep  clearly  in 
mind  the  fact  that  all  pra'cordial  or  so-called  heart-pains  are  not 
attacks  of  angina  pectoris.  Many  of  these  pains  are  simple  inter- 
costal neuralgias,  and  although  variously  described  as  cutting, 
stabbing,  tearing,  shooting,  darting,  l)urning,  smarting,  or  only  as 
dull,  sore,  heavy,  and  the  like,  they  lack  two  features  essential  to 
angina  pectoris — namely,  the  feeling  of  the  chest  being  crushed, 
and  the  sense  of  the  near  presence  of  deatli. 

The  fact  that  pain  is  felt  in  the  region  of  the  left  nipple  or 
that  it  radiates  from  that  point  into  the  left  shoulder  and  arm  does 
not  warrant  the  conclusion  that  it  is  angina.  Indeed,  a  pain  that 
takes  its  jK)iiil  df  departure  at  llic  stcnud  end  of  the  fourth  left 
interspace  or  iji  tlie  fifth  left  intersj)ace  below  the  breast,  whatever 


ANGINA  PECTORIS  G55 

be  its  direction  of  radiation,  is  more  likely  to  be  an  intercostal 
neuralgia,  since  the  agonizing  suffering  meriting  the  name  .angina 
pectoris  is  most  frequently  substernal.  MoreoV'Cr,  in  cases  of  in- 
tercostal neuralgia  there  are  usually  well-defined  tender  spots  cor- 
resi)onding  to  the  points  of  origin  of  the  pain.  Another  character- 
istic of  these  intercostal  neuralgias  is  their  coming  like  a  sudden 
stab  or  thrust,  and  then  leaving  as  quickly,  the  points  where  they 
aj)peared  being  sore  to  the  touch.  When,  as  in  some  instances,  the 
pain  is  permanent  or  is  continuous,  with  exacerbations  and  remis- 
sions, the  very  length  of  the  attack  stamps  it  as  intercostal  neural- 
gia and  not  angina  pectoris. 

Moreover,  these  jjains  are  most  frequently  met  with  in  anae- 
mic, neurasthenic,  or  otherwise  neurotic  individuals,  or  such  as 
present  symptoms  of  gastric  disorder,  and  although  by  no  means 
limited  to  the  female  sex,  they  are  more  frequent  in  women  than 
in  men,  and  generally  in  such  as  have  not  yet  reached  the  age  at 
which  vascular  degenerations  are  to  be  expected.  In  most  cases 
attention  to  the  points  just  mentioned  enables  one  to  readily  differ- 
entiate intercostal  neuralgias  from  the  true  heart-pain  of  angina. 
It  is  far  otherwise,  however,  with  those  attacks  of  prsecordial  pain 
which  display  the  features  of  true  angina  pectoris,  yet  which  in 
reality  do  not  belong  to  that  class. 

In  other  words,  is  it  Heberden's  angina  with  its  possibility  of 
sudden  death  ?  or  is  the  pain  a  pseudo-angina,  and  hence  not  of  the 
same  serious  import  ?  The  answer  to  these  queries  is  to  be  found 
in  the  consideration  of  the  following  points:  (1)  the  age  and  sex 
of  the  individual,  (2)  the  state  of  the  arteries  and  heart,  (3)  the 
influence  of  effort  in  evoking  a  paroxysm. 

Attacks  of  prsecordial  pain  that  occur  in  young  persons,  no 
matter  how  closely  they  resemble  coronary  angina,  are  presumably 
symptomatic  of  irritation  in  some  other  organ  than  the  heart,  and 
if  such  attacks  are  in  women  the  presumption  is  the  stronger  that 
they  are  false  angina.  If,  on  the  contrary,  they  occur  at  an  age 
when  vascular  degeneration  is  common,  they  are  much  more  likely 
to  be  of  the  grave  kind,  even  though  they  occur  in  females. 

The  detection  of  stiff  arteries  or  of  signs  of  heart-disease  is  in 
favour  of  true  angina,  and  jet  pain  of  visceral  disturbance  may 
occur  in  women  past  forty  with  hypertrophied  hearts,  particularly 
at  the  menopause  or  in  such  as  have  suffered  all  their  life  from 


656  DISEASES  OP   THE   HEART 

constipation  and  defective  elimination.  The  same  thing  may  be 
said  of  young  persons  of  either  sex  who  long  before  they  reach 
forty  are  victims  of  aortic  valvular  disease. 

Consequently  in  all  such  cases  particular  attention  is  to  be 
paid  to  the  influence  of  pli^'sical  exertion  over  the  attacks  of  pain. 
If  the  initial  paroxysm  took  place  during  exercise,  if  the  pain  is 
aroused  by  a  hurried  walk  or  by  walking  after  a  meal  or  against 
a  cold  damp  wind,  if  it  compels  the  patient  to  stop  in  his  tracks 
and  remain  standing  until  it  passes  away,  it  is  in  all  probability 
a  true  angina.  If,  on  the  other  hand,  the  person  is  able  to  con- 
tinue his  walk,  if  he  sits  or  lies  down,  instead  of  standing,  during 
the  acme  of  the  pain,  and  if  he  is  restless,  moaning,  and  throwing 
himself  about,  the  attack  is  probably  one  of  pseudo-angina  pec- 
toris. 

In  cases  of  a  mixed  nature  described  by  Huchard,  in  which 
cardiac  or  vascular  disease  is  complicated  with- attacks  of  pain  of 
an  hysterical  nature,  there  is  often  great  difficulty  of  diagnosis. 
Their  precise  nature  can  only  be  determined  by  noting  carefully 
the  influence  of  effort  in  provoking  the  seizures  and  by  the  discov- 
ery of  the  stigmata  of  hysteria. 

Furthermore,  in  attempting  to  distinguish  the  false  from  the 
true  angina,  one  should  never  forget  that  the  occurrence  of  pain 
alone  is  not  sufficient  for  a  trustworthy  diagnosis,  but  that  the 
symptom-complex  of  pain,  constriction  of  the  chest  and  a  sense  of 
impending  death,  is  essential.  Pain  is  the  paramount  sensation, 
but  in  typical  coronary  angina  there  is  more  or  less  blending  of 
the  other  two.  There  are  doubtless  horder-line  cases,  as  they  may 
be  called,  in  which  it  is  impossible  to  assert  positively  the  real 
nature  of  the  pain,  especially  in  elderly  well-to-do  males  with  stiff 
arteries,  yet  in  whom  constriction  and  the  feeling  of  overhanging 
death  are  wanting  or  not  pronounced.  If,  on  the  other  hand,  the 
patient  is  young  and  a  female  and  the  two  symptoms  just  men- 
tioned are  absent,  tlie  pain  may  quite  safely  be  set  down  as  a  false 
angina  pectoris. 

Finally,  the  pathological  condition  underlying  the  angina  is  to 
be  determined  so  far  as  possible.  Thickened  arteries  in  a  person 
past  forty  and  signs  of  sclerosis  of  the  aorta  should  be  carefully 
sought  for.  Curschmann  has  pointed  out  that  tlic  elongation  and 
widening  of  the  arch  incident  to  sclerotic  changes  may  be  recog- 


■^      ANGINA  PECTORIS  657 

nised  by  careful  study  of  the  cervical  arteries.  In  the  fossa  jugu- 
laris,  particularly  during  the  act  of  swallowing,  may  be  seen,  or, 
still  better,  felt  the  pulsation  of  the  transverse  portion  of  the 
aorta,  while  the  pulsation  of  the  subclavians  is  situated  abnor- 
mally high  and  the  carotids  arch  unnaturally  forward  and  feel 
stiff  and  perhaps  slightly  irregular.  There  may  be  slight  dulness 
at  right  of  the  sternum,  appreciable  only  upon  deep  percussion, 
and  the  second  aortic  tone  is  sharp  and  ringing.  The  detection 
of  such  signs  would  strongly  support  the  conclusion  that  the 
angina  was  due  to  coronary  degeneration,  and  was  therefore  most 
grave. 

Musser  has  reported  a  series  of  cases  in  which  there  was  typi- 
cal anginal  seizures  so  long  as  the  left  ventricle  was  hypertrophied, 
yet  in  which  with  supervention  of  dilatation  the  attacks  of  pain 
disappeared.  These  observations  have  led  Musser  to  conclude  that 
in  some  cases  angina  pectoris  is  due  to  increased  intracardiac 
blood-pressure.  In  all  such  instances  the  exact  nature  of  the 
underlying  condition  cannot  be  made  with  certainty,  and  one  must 
content  himself  with  the  diagnosis  of  the  angina  and  of  the  car- 
diac condition  without  attempting  to  do  more  than  speculate  on 
the  connection  between  the  two. 

Prognosis. — As  has  been  repeatedly  stated,  there  is  always 
a  possibility,  and,  according  to  Huchard,  a  strong  probability  of 
sudden  death  in  a  paroxysm  of  angina  pectoris.  Even  if  the 
patient  does  not  succumb  during  an  attack,  the  complaint  is  in- 
curable. He  should  be  advised,  therefore,  concerning  the  gravity 
of  his  affection,  and  his  immediate  family  should  be  warned  of 
the  likelihood  of  a  fatal  termination.  How  long  a  patient  is 
likely  to  live,  subject  to  these  attacks,  is  a  matter  of  too  great 
uncertainty  for  an  expression  of  opinion  by  a  prudent  physician. 
It  is  always  well  to  reassure  the  sufferer,  however,  by  the  state- 
ment that  patients  have  been  known  to  experience  the  symptom 
for  a  long  term  of  years,  and  that  its  severity  and  the  frequency  of 
its  occurrence  are  likely  to  be  modified  by  appropriate  medical 
treatment  and  by  the  care  exercised  by  the  patient. 

Other  things  being  equal,  it  may  be  said  that  the  more  severe 
the  attacks  the  greater  the  danger  of  death.  Also,  the  more  easily 
the  paroxysms  are  evoked,  the  more  extensive  is  the  coronary  ob- 
struction, and  the  graver  the  complaint.  Increasing  frequency  of 
48 


658  DISEASES  OF  THE  HEART 

recurrence  is  likewise  of  evil  import.  On  the  contrary,  the  prog- 
nosis may  be  said  to  improve  in  proi)ortion  as  the  attacks  become 
less  severe  and  the  intervals  between  them  longer. 

According  to  Powell's  assumption,  previously  mentioned,  the 
prognosis  should  be  better  when  relief  is  afforded  by  slow  walking, 
but  the  case  I  have  cited  of  the  attorney  proves  the  contrary. 
Moreover,  in  the  case  of  my  other  patient  his  condition  grew  stead- 
ily worse  in  spite  of  his  ability  to  endure  the  exercises  to  which 
he  resorted  in  the  vain  hope  of  improving  his  general  health,  since 
his  attacks  of  pain  became  more  frequent  if  not  more  intense. 

Treatment. — This  includes,  first,  measures  addressed  to  the 
relief  of  the  paroxysms,  and  second,  the  management  of  the  pa- 
tient's daily  life  during  the  intervals  between  the  seizures,  with  a 
view  if  possible  to  lessening  their  frequency  and  severity.  The 
treatment  of  the  attacks  has  already  been  considered  in  the  chap- 
ter dealing  with  myocardial  diseases  secondary  to  coronary  scle- 
rosis, but  may  be  again  discussed  at  this  time  at  somewhat  greater 
length. 

Very  many  and  divers  remedies  have  been  used  either  solely 
to  relieve  the  pain,  or  to  strengthen  and  regulate  the  heart's  action, 
and  are  therefore  either  anodynes  or  stimulants.  Inhalations 
of  chloroform  and  ether,  Hoffman's  anodyne,  aromatic  spirits  of 
ammonia,  opiates,  carminative  draughts,  such  were  the  measures 
relied  upon  prior  to  the  discovery  and  introduction  by  Richardson 
and  Lauder  Brunton  of  nitrite  of  amyl.  Two  medicaments  which 
in  the  experience  of  the  profession  the  world  over  have  proved  of 
tlie  liighest  value  in  controlling  the  attacks  of  angina  pectoris, 
and  now  universally  employed,  are  the  nitrites  and  opium.  The 
action  of  the  nitrite  of  sodium  is  too  slow,  and  therefore  Ave  have 
recourse  either  to  the  inhalation  of  a  few  drops  of  nitrite  of  amyl, 
or  to  a  minim  of  a  1-per-cent  solution  of  nitroglycerin  dropped  on 
the  tongue.  If  amyl  nitrite  is  preferred,  it  should  be  carried  about 
by  the  patient  in  the  form  of  nitrite-of-amyl  pearls,  containing 
3  to  5  minims  each  of  the  remedy.  Kept  in  this  way  the  drug 
does  not  lose  strength.  So  soon  as  the  patient  perceives  his  pain 
a  pearl  is  to  be  crushed  in  the  handkerchief,  or  a  few  drops  from 
a  vial  may  be  poured  thereon  and  the  fumes  inhaled,  or  the  suf- 
ferer may  breathe  them  directly  from  the  vial.  The  action  of 
the  remedy  is  usually  very  prompt,  rarely  failing  to  afford  relief. 


ANGINA  PECTORIS  659 

There  is  usually  no  danger  attending  its  use;  at  the  most,  only  a 
dull  headache  is  produced.  If  nitroglycerin  be  preferred,  it  is 
most  conveniently  and  usually  administered  in  the  form  of  a 
tablet  triturate  containing  1  minim  of  a  1-per-cent  solution.  If 
the  tablet  is  dissolved  on  the  tongue  instead  of  being  swallowed,  its 
effect  is  more  promptly  induced.  This  is  especially  the  case  if 
the  occasion  for  its  use  is  soon  after  the  taking  of  food.  The 
remedy  can  also  be  dropped  on  the  tongue  or  taken  in  a  swallow  of 
water  when  the  solution  is  preferred,  but  this  method  is  not  only 
less  convenient,  but  it  necessitates  the  loss  of  valuable  time,  when 
seconds  of  agony  seem  like  hours  to  the  sufferer. 

Abatement  or  cessation  of  the  attack  generally  takes  place  in 
a  few  seconds ;  but  should  this  not  be  the  case  a  second  or  even  a 
third  tablet  may  be  employed  at  intervals  of  two  or  three  minutes. 
Special  indications  for  one  or  another  of  these  remedies  are  found 
in  pallor  of  the  countenance  and  a  small  and  tense  pulse,  whether 
slow  or  accelerated,  regular  or  irregular,  and  intermittent  or  not, 
and  in  other  signs  of  arterial  spasm.  The  nitrites  are  essentially 
vaso-dilators,  and  stimulate  the  heart  only  indirectly  through  their 
dilating  influence  on  the  arterioles.  Through  their  action,  the 
wiry,  and  it  may  be  slow,  pulse  grows  softer,  fuller,  and  more 
rapid,  while  at  the  same  time  there  may  be  felt  some  constriction 
of  the  throat  and  tense  or  throbbing  headache,  spnptoms  which 
to  the  patient  are  of  small  moment  in  comparison  with  the  relief 
from  his  frightful  agony. 

It  has  generally  been  my  observation  that  in  elderly  individ- 
uals with  sclerosis  of  the  temporal,  and  presumably  therefore  of 
the  cerebral  arteries,  the  head  symptoms  occasioned  by  the  nitrites 
are  far  less  pronounced  than  in  younger  persons  whose  vessels  are 
less  stiff,  and  hence  more  responsive  to  the  action  of  the  drug. 
When  phenomena  of  vascular  spasm  are  absent  or  when  relief  does 
not  promptly  follow  the  use  of  the  nitrites,  recourse  would  better 
be  had  to  opium  in  some  form.  A  method  of  administration  that 
yields  speedy  results  is  indicated,  and  therefore  it  is  best  to  give 
morphine  hypodermically  and  in  a  dose  that  will  suffice  without 
repetition — e.  g.,  ^  or  even  -|  of  a  grain. 

X  The  lady  to  whom  reference  has  been  repeatedly  made  was 
compelled  to  resort  to  both  nitroglycerin  and  morphine,  and  in 
addition  frequently  took  a  teaspoonful  of  sulphuric  ether  in  sweet- 


H60  DISEASES  OP  THE  HEART 

eiied  iec-watcr.  Ivclief  was  not  obtained  initil  under  their  com- 
bined effect  the  pnlse  became  fnll  and  bonnding,  and  the  skin,  pre- 
viously cold  and  perspiring,  grew  flushed  and  warm.  In  her  case 
there  was  extreme  aortic  stenosis  with,  it  may  be,  coronary  scle- 
rosis, and  a  more  decided  stimulation  of  the  heart  was  required 
than  was  indirectly  occasioned  by  nitroglycerin.  Under  the  influ- 
ence of  the  ether,  cardiac  contractions  are  both  invigorated  and 
quickened,  so  that  the  coronaries  previously  dilated  by  nitroglyc- 
erin receive  a  more  adequate  supply  of  blood. 

In  comparatively  mild  cases  relief  may  sometimes  be  obtained 
by  the  administration  of  diff'usible  stimulants,  as  aromatic  spirits 
of  ammonia,  Hoffman's  anodyne,  camphor,  whisky,  or  brandy, 
and  their  effect  is  hastened  by  being  taken  in  hot  water.  Elixir 
of  valerianate  of  anmionia  in  tcaspoonful  doses  is  a  particularly 
eligible  ])reparation,  and  admirably  meets  the  indications  when 
rapid  stimulation  is  required.  Any  one  of  these  remedies  may 
be  administered  directly  following  the  nitroglycerin  and  Mill 
sometimes  obviate  the  necessity  for  morphine,  a  consideration  of 
some  importance  in  elderly  individuals  who,  as  well  known,  arc 
sometimes  peculiarly  sensitive  to  this  drug. 

In  nocturnal  attacks,  which  are  apt  to  be  severe  and  prolonged, 
it  is  often  well  to  supplement  the  action  of  medicinal  agents  by 
the  application  of  hot  bottles  to  the  extremities  or  by  heat  to  the 
pnpcordium,  the  epigastrium,  or  between  the  shoulders.  There  is 
no  indication  during  an  attack  for  the  use  of  digitalis  and  strych- 
nine, for  not  only  is  their  action  too  slow,  but  when  arterial  S])asm 
is  responsible  for  the  paroxysm  the  former  will  do  harm.  Aco- 
nite and  veratrum  viride  should  never  be  employed  at  such  a  time. 

During  the  intervals  between  attacks  the  daily  life  of  the  pa- 
tient should  be  so  regulated  as  to  minimize  if  possible  both  the  fre- 
quency and  severity  of  his  seizures.  If  the  complaint  has  existed 
for  some  time  the  sufferer  is  likely  to  have  learned  by  experience 
that  moderation  in  tlu;  matter  of  exercise  is  absolutely  indispensa- 
ble to  iiiiiinuiity  from  his  attacks.  Nevertheless  it  may  be  well 
to  caution  him  against  undue  exposure  during  cold  and  inclement 
weather,  or  going  about  insufticiently  clad,  against  carrying  heavy 
hand  l)aggage  or  parcels,  against  attem])ting  to  walk  soon  aft^r  a 
meal,  hurrying  to  catch  a  train  or  street  car,  etc.  He  should  l)o 
explicitly  instructed  to  make  use  of  surface  transportation  in  pref- 


ANGINA  PECTORIS  OGl 

oreiK'o  to  elevated  roads,  which  have  to  be  reached  by  long  flights 
of  stairs,  since  the  inclination  to  hasten  Tip  the  last  few  steps  as 
the  train  is  heard  approaching  is  almost  irresistible,  and  such  a 
spurt  may  precipitate  an  attack.  Patients  should  also  be  in- 
structed concerning  the  harmfulness  of  immoderate  coitus,  fits  of 
passion,  overeating,  the  too  free  indulgence  in  tobacco  and  alco- 
holic stimulants,  of  becoming  excessively  fatigued,  etc. 

The  hands  and  feet  should  be  kept  warmly  covered,  and  it  is 
often  well  for  these  patients  to  wear  a  chest-protector  both  front 
and  back.  Those  who  can  afford  to  pass  the  inclement  seasons  in 
a  warm,  equable  climate  should  be  advised  to.  do  so,  since  they 
can  there  take  outdoor  exercise  without  fear  of  encountering  cold 
winds  and  of  contracting  attacks  of  bronchitis. 

Sufferers  from  coronary  angina  have  habitually  high  and  sus- 
tained arterial  tension,  and  as  it  is  sudden  and  unexpected  aug- 
mentation of  this  tension  which  often  precipitates  a  paroxysm,  it 
is  essential  that  their  blood-pressure  be  lowered.  This  can  usually 
be  accomplished,  in  a  measure  at  least,  by  revision  of  the  dietary 
— that  is,  by  the  restriction,  or  in  some  instances  by  the  exclusion, 
of  meats  and  the  substitution  of  a  largely  vegetable  dietary. 

E,umpf,  of  Hamburg,  interdicts  the  use  of  foods  rich  in  lime- 
salts,  as  eggs,  milk,  cheese,  spinach,  etc.  Theoretically,  such  a 
restriction  is  called  for  when  there  is  arteriosclerosis,  but  practi- 
cally, it  will  be  found  difficult  to  adequately  nourish  the  patient 
if  all  foods  rich  in  phosphates  as  well  as  meats  are  excluded. 
Turthermore,  a  too  restricted  dietary  grows  monotonous  and  leads 
to  anorexia  and  feeble  digestion. 

The  principles  laid  down  for  the  dietary  of  cases  of  myocar- 
dial degeneration  are  equally  applicable  to  these  patients,  and 
therefore  the  reader  is  referred  to  that  chapter  for  details.  Should 
arterial  tension  be  not  sufficiently  reduced  by  regulation  of  the 
diet,  then  attempts  must  be  made  to  accomplish  this  in  other  ways. 
To  this  end  appropriate  doses  of  nitroglycerin  may  be  given  every 
two  or  three  hours  during  the  day,  or  moderate  doses  of  an  iodide 
salt,  three  times  daily,  may  accomplish  the  result.  That  such  is 
the  effect  of  iodine  internally  is  generally  held,  and  yet  Komberg 
asserts  that  both  clinical  observation  and  experiment  show  this 
not  to  be  the  case.  In  some  cases  it  may  not  be  necessary  to  give 
nitroglycerin  daily,  but  only  on  those  days  when  the  patient  finds 


662  DISEASES  OF  THE   HEART 

walking  particularly  difficult,  or  there  is  a  raw  easterly  wind.  I 
have  known  striking  amelioration  of  the  patient's  condition  follow 
regulation  of  the  diet,  together  with  the  prolonged  use  of  nitro- 
glycerin and  iodide  of  soda.  Men  addicted  to  the  use  of  tobacco 
should  be  informed  of  its  baneful  effects  and  advised  to  abandon 
the  habit  altogether.  If  this  is  not  acceded  to,  then  the  matter 
may  be  compromised  by  the  patient's  being  allowed  to  smoke 
only  mild  domestic  cigars.  This  will  sometimes  affect  a  cure  of 
the  tobacco  habit  in  those  who  have  been  accustomed  to  choice 
Ilavanas. 

In  cases  that  have  begun  to  manifest  cardiac  insufficiency  or 
in  which  abnormally  high  blood-pressure  threatens  to  soon  over- 
power the  heart,  attempts  must  be  made  to  restore  cardiac  strength 
or  at  least  to  stay  its  further  decline.  To  this  end  recourse  may  be 
had  to  the  usual  heart-tonics.  Strophanthus  appears  to  me  prefer- 
able to  digitalis  by  reason  of  its  inferior  constricting  effect  on  the 
arterioles,  a  virtue  of  the  drug  to  which  Frazer  originally  directed 
attention.  If  digitalis  is  selected,  then  its  vaso-constrictor  effect 
must  be  offset  by  the  iodides  or  nitroglycerin.  Strychnine  and 
arsenious  acid  are  also  of  benefit,  and  the  former  may  be  continued 
in  moderate  doses  for  many  months.  Strychnine  is  generally  be- 
lieved to  raise  pulse-tension,  but  this  action  is  slight  and  not  to  be 
weighed  in  the  balance  as  against  its  value  as  a  heart-tonic. 

The  one  method  of  treatment  that  is  particularly  adapted  to 
this  class  of  patients  at  this  time  are  the  so-called  resistance  exer- 
cises, and  very  favourable  results  have  been  reported  from  their 
employment  in  angina  pectoris.  Theoretical  considerations,  and 
indeed  actual  experience,  indicate  that  benefit  is  also  likely  to  fol- 
low the  careful  use  of  the  saline  baths  with  artificial  as  well  as 
natural  waters.  iN^evertheless,  the  lady  whose  case  has  been  so 
often  cited  in  these  pages  experienced  her  first  severe  paroxysm 
of  angina  pectoris  shortly  after  her  first  bath  at  Bad  Nauheim 
upon  having  been  wheeled  to  her  hotel,  and  then  attempting  to 
walk  slowly  from  her  wheel-chair  to  the  elevator  on  her  way  to  her 
apartments.  Subsequent  baths,  however,  were  not  followed  by  a 
similar  distressful  effect.  Details  concerning  this  mode  of  treat- 
ment are  found  elsewhere.  (See  chapter  on  Treatment  of  Valvu- 
lar Disease  in  General.) 


CHAPTER  XXVI 

SYPHILIS  OF  THE  MYOCARDIUM  — NEW  GROWTHS 
IN  THE  MYOCARDIUM— ATROPHY  OF  THE  HEART 
—SEGMENTATION  AND  FRAGMENTATION  OF  THE 
MYOCARDIUM 

I.   SYPHILIS  OF   THE   MYOCARDIUM 

Morbid  Ana-tomy. — The  most  common  myocardial  mani- 
festation of  syphilitic  infection  consists  in  fatty  degeneration  of 
the  cardiac  muscle.  This  is  not  different  in  any  way  from  fatty 
degeneration  from  other  causes,  and  so  is  not  recognisable  except  in 
the  presence  of  other  evidences  of  the  disease.  Associated  with 
the  arteriosclerosis  of  syphilis  is  a  diffuse  interstitial  myocarditis, 
which  is  also  usually  classed  as  a  luetic  lesion.  It  seems  probable, 
however,  that  in  many  cases  the  induration  is  due  to  the  presence 
of  the  arterial  disease,  rather  than  to  the  direct  action  of  the 
syphilitic  poison. 

Gumma  of  the  heart  is  very  rare,  and  especially  so  in  the  con- 
genital form  of  the  affection.  The  part  of  the  heart  most  com- 
monly affected  is  the  wall  of  the  left  ventricle.  The  gummata 
appear  as  soft  grayish  masses  surrounded  by  hyperplastic  fibrous 
tissue,  or  if  older,  as  dry  caseous  areas  of  a  yellowish  white  colour. 
Very  rarely  a  softening  gumma  may  rupture  into  one  of  the  cavi- 
ties of  the  heart. 

Etiology. — Syphilis  attacks  the  myocardium  only  in  the  ter- 
tiary period  of  the  disease,  and  after  a  lapse  of  five  or  ten  years  or 
longer  following  the  initial  sore.  It  is  not  confined  to  either  sex, 
but  appears  to  have  been  rather  more  frequently  discovered  in 
males.  As  regards  age,  it  may  be  said  to  be  more  frequent  at  or 
after  middle  life,  rarely  in  childhood  for  the  reason  that  the  dis- 
ease is  generally  acquired,  not  congenital. 

663 


664  DISEASES   OF   THE   HEART 

Symptoms. — Xot  only  is  heart-syphilis  a  comparatively  rare 
affection,  having  been  for  the  first  time  detected  by  Ricord,  but 
its  clinical  recognition  is  still  less  frequent  than  is  its  post-mortem 
discovery.  This  is  due  to  the  fact  of  its  possessing  no  pathogno- 
monic features  as  yet  recognised.  Not  only  have  patients,  in  whom 
this  myocardial  disease  has  been  discovered  after  death,  been 
known  to  exhibit  no  clinical  evidence  of  heart-affection  during 
life,  but  when  symptoms  were  present  they  were  found  on  analysis 
to  differ  in  nowise  from  those  displayed  by  persons  suffering  from 
other  non-syphilitic  forms  of  myocardial  degeneration.  Most  ob- 
servers agree  in  this  statement  that  the  cardiac  action  is  likely  to 
be  disordered.  This  is  generally  though  not  invariably  acceler- 
ated, and  some  authors,  as  Semmola,  lay  great  stress  on  arrhyth- 
mia and  acceleration  of  the  pulse.  Another  symptom  that  has 
been  noted  is  an  indescribable  prircordial  distress  which  may  or 
may  not  amount  to  actual  pain.  Philips  has  called  attention  to 
angina-like  pain  as  having  been  present  in  one  or  two  cases  ob- 
served by  him.  This  symptom  was  remarkably  distressing  on  one 
occasion  in  a  professional  man,  who  subsequently  died  suddenly 
and  in  whom  Philips  found  syphilis  of  the  myocardium  at  the 
autopsy.  Cardiac  dyspnoea  has  also  been  complained  of  by  some 
patients,  but  there  was  nothing  about  the  difficulty  of  breathing 
that  was  in  anywise  peculiar. 

Upon  examination  of  the  patient  there  may  or  may  not  be 
evidence  of  specific  infection,  such  as  old  scars  on  the  skin  or 
mucous  membranes,  glandular  induration,  gummata,  etc.,  and  the 
arterial  system  may  or  may  not  furnish  evidence  of  sclerosis. 
Physical  examination  of  the  heart  is  not  infrequently  negative, 
while  in  some  cases  there  are  signs  of  cardiac  disease.  When  these 
are  present,  they  are  apt  to  be  those  of  dilatation  with  feebleness 
or  altered  quality  of  the  sounds,  ^rurniurs  are  not  ])rcsent  as  a 
rule  unless  as  an  accidental  complication  or  due  to  the  dilatation — 
i.  e.,  to  relative  insufficiency  of  the  mitral  valves,  for  example. 

Diagnosis. — Unless  there  is  a  clear  history  of  previous 
sypliililic  infection  the  diagnosis  of  myocardial  syphilis  is  not  pos- 
sible with  certainty.  On  the  other  hand,  even  with  such  a  history, 
one  is  not  always  justified  in  making  the  diagnosis  merely  because 
an  individual  of  middle  age  disjilays  cardiac  symptoms.  They 
may  be  due  to  changes  in  the  heart-muscle  incident  to  his  age  and 


SYPHILIS  0^  THE  MYOCARDIUM  665 

not  at  all  to  sypliilis.  If  one  cannot  discover  sypbilides  of  one  sort 
or  another,  he  should  give  the  patient  the  benefit  of  the  doubt  until 
the  futility  of  all  other  modes  of  treatment  has  been  proved.  The 
association  of  symptoms  and  signs  of  myocardial  disease  with  a 
history  and  with  clearly  demonstrable  lesions  of  the  specific  in- 
fection renders  the  existence  of  syphilis  of  the  heart-wall  very 
probable.  If  the  cardiac  manifestations  occur  in  an  individual 
not  yet  fifty  years  of  age  the  supposition  is  greatly  strengthened. 
Very  often  the  diagnosis  will  have  to  be  deferred  until  the  results 
of  specific  treatment  have  been  ascertained.  Except  by  men  of 
wide  exj)erience  in  this  particular  line  of  diseases  the  diagnosis 
of  this  cardiac  affection  must  necessarily  be  a  matter  of  guesswork 
in  most  instances.  The  clinical  obscurity  enveloping  this  affection 
is  shown  by  the  relative  frequency  with  which  it  is  found  at  the 
autopsy  as  compared  with  its  intra  vitani  recognitioji. 

Prognosis. — This  may  be  said  to  be  good  provided  the  disease 
is  recognised  in  time  to  institute  proper  treatment.  In  undiag- 
nosed cases  the  prognosis  is  bad,  since  they  are  likely  to  terminate 
fatally.  Death  is  apt  to  be  sudden  and  unexpected.  I  know  of  no 
statistics  going  to  show  how  long  may  be  the  duration  of  the  dis- 
ease, but  it  is  probably  a  very  chronic  affection,  having  existed 
years,  it  may  be,  before  the  coming  on  of  cardiac  symptoms.  The 
rapidity  with  which  death  is  likely  to  follow  the  development  of 
symptoms  is  likewise  a  matter  of  individual  difference  depending 
on  the  extent  of  the  myocardial  change,  which  is  itself  a  matter 
we  cannot  obtain  definite  knowledge  of  during  life.  If  the  heart 
be  extensively  dilated,  its  action  greatly  disturbed,  and  the  pa- 
tient's symptoms  pronounced,  the  prognosis  is  grave,  and  even 
specific  treatment  is  not  likely  to  do  more  than  effect  a  partial 
recovery. 

Treatment. — This,  it  needs  hardly  be  stated,  is  the  employ- 
ment of  iodides,  with  or  without  mercurials,  as  the  physician  de- 
termines. Being  a  tertiary  manifestation,  reliance  is  to  be  placed 
chiefly  on  the  iodides.  Ordinarily  other  remedies  of  the  class  of 
cardiac  tonics  are  not  necessary.  But  here  again  the  medical  ad- 
viser must  decide.  Their  employment  is  symptomatic,  and  digi- 
talis in  conjunction  with  the  specific  medication  may  be  of  service 
in  cases  in  which  the  action  of  the  heart  is  much  deranged  and 
the  patient's  distress  from  dyspnoea  is  considerable.     What  has 


666  DISEASES  OF  THE  HEART 

been  said  in  other  chapters  on  the  hygienic  management  of  heart 
patients  applies  equally  to  these,  so  long  as  cardiac  power  is  de- 
ficient. 

II.    NEW  GROWTHS  IN  THE  MYOCARDIUM 

Under  this  head  are  included  various  tumours  and  parasites. 
They  are  rare,  some  of  them  as  parasites  being  excessively  so, 
and  aside  from  gummata  just  considered  possess  interest  for  the 
pathologist  rather  than  the  clinician.  They  will  therefore  receive 
only  brief  mention  in  this  work. 

Tubercles  of  the  myocardium  may  be  encountered  as  miliary 
nodules  scattered  through  the  heart-muscle,  or  still  more  rarely 
as  caseous  masses.  The  affection  may  also  be  declared  as  an  inter- 
stitial myocarditis,  which,  however,  possesses  no  distinctive  fea- 
tures. 

Parasites  and  cysts  in  this  situation  are  still  more  infrequent 
and  usually  fail  to  declare  their  presence  by  either  subjective  or 
objective  symptoms.  Thus  Knaggs,  in  the  Lancet  of  1896,  vol.  i, 
p.  29,  narates  the  instance  of  a  man  who  died  suddenly,  and 
had  not  previously  manifested  evidence  of  cardiac  disease,  yet  in 
the  wall  of  whose  left  ventricle  a  hydatid  cyst  was  found  at  the 
necropsy. 

Of  other  growths  in  the  myocardium  cancer  is  the  most  fre- 
quent, and  yet  this  is  absolutely  very  uncommon.  Lipoma  and 
fibroma  have  also  been  met  with,  but  are  still  more  rare.  Ma- 
lignant tumours  occur  in  either  the  primary  or  secondary  form, 
but  of  the  two  the  latter  is  much  the  more  frequent.  The  rarity 
of  the  primary  form  may  be  judged  of  by  Gibson's  statement  that 
in  21,954  autopsies  mentioned  by  Koehler,  Tanchon,  and  Willigk 
there  were  only  21  instances  of  heart-cancer,  while  Petit  found 
but  7  in  the  literature. 

From  Bodenheimer's  analysis  of  45  cases  of  secondary  can- 
cer, also  cited  by  Gibson,  it  appears  that  the  growth  occurs  most 
often  as  multiple  nodules  scattered  throughout  the  myocardium, 
since  it  was  limited  to  the  wall  of  the  left  ventricle  but  seven  times, 
to  that  of  the  right  ventricle  three  times,  and  to  the  right  auricle 
twice.  It  may  occur  at  any  age,  even  in  infancy,  but  most  often 
after  forty-five,  and  is  more  frequent  in  males. 

The  clinical  manifestations  of  myocardial  cancer  are  too  in- 


ATROPHY   OF   THE   HEART  667 

definite  and  uncertain  to  permit  an  intra-vitam  diagnosis.  The 
heart  may  be  irregular  and  feeble  in  action,  may  furnish  percus- 
sion evidence  of  dilatation,  but  in  such  findings  there  is  nothing 
to  distinguish  these  from  ordinary  cases  of  myocardial  degen- 
eration. 

The  prognosis  is  unfavourable,  and  yet  for  the  most  part  life 
is  destroyed  in  secondary  cases  by  the  original  disease.  In  pri- 
mary heart-cancer  the  tenure  of  life  will  depend  largely  upon  the 
seat  and  nature  of  the  tumour. 

Treatment  is  of  course  purely  symptomatic,  since  if  the  ac- 
tion of  the  heart  is  disordered  and  the  real  cause  of  the  disorder  is 
unsuspected  or  not,  physicians  find  themselves  limited  to  the 
administration  of  heart-tonics. 

III.    ATROPHY   OF   THE  HEART 

By  atrophy  of  the  heart  is  meant  a  diminution  of  the  organ 
in  weight  and  size.  The  condition  may  be  partial  or  general. 
The  former  is  exemplified  in  the  smallness  of  the  left  ventricle 
seen  in  extreme  mitral  stenosis. 

General  atrophy  may  be  the  result  of  age,  when  it  is  spoken 
of  as  physiological,  or  the  effect  of  disease — i.  e.,  pathological. 
Congenital  smallness  of  the  heart  is  sometimes  designated  as 
atrophy,  but,  as  preferred  by  Virchow,  should  be  properly 
termed  hypoplasia  of  the  heart.  It  is  usually  associated  with  con- 
genital smallness  of  the  genitalia. 

Morbid  Anatomy. — The  atrophied  heart  is  of  a  brownish 
red  or  yellowish  colour,  often  firmer  than  normal,  sometimes  pre- 
senting a  wrinkled  appearance,  owing  to  puckering  of  the  epicar- 
dium  (like  a  withered  pear,  Eichhorst);  and  beneath  the  micro- 
scope the  individual  muscle-fibres  are  seen  to  be  diminished  in 
size,  their  transverse  striation  obscured  and  stained  by  a  deposit 
of  brown  or  yellow  pigment  near  their  nuclei.  Adipose  tissue  is 
everywhere  absent. 

Etiology. — Various  causes  of  general  cardiac  atrophy  are 
enumerated,  but  those  most  often  and  powerfully  operative  are 
conditions  which  induce  marasmus — i.  e.,  pulmonary  phthisis, 
cancer,  diabetes,  and  chronic  suppuration,  as  from  disease  of  a 
bone.  Thus  W.  Church  is  said  to  have  obtained  from  the  body  of 
a  woman  who  died  of  slow  starvation  in  consequence  of  pylorus 


668  DISEASES   OF  THE  HEART 

obstruction  by  eareinoivia  a  heart  tliat  woii>,lio(l  only  P)-^^  oinices. 
Of  ]71  cases  of  phthisis  analyzed  by  (^iiain  the  heart  was  atro- 
phied in  54.4  per  cent,  ^\diile  Engel  is  reported  to  have  found 
cardiac  atrophy  in  about  25  per  cent  of  males  who  died  of  the 
same  wasting  disease  between  the  ages  of  twenty-eight  and  thirty. 
It  may  here  be  stated  that,  according  to  Wunderlich,  a  heart  is  to 
be  regarded  as  atrophied  if  it  weighs  less  than  200  grammes. 

Symptoms. — The  clinical  manifestations  of  atrophy  of  the 
myocardium  are  obscured  by  those  of  the  general  complaint,  but 
may  be  said  to  be  such  as  always  characterize  cardiac  inadequacy 
— i.  e.,  rapidity  and  weakness  of  the  pulse,  feebleness  of  cardiac 
impulse  and  sounds,  without,  however,  signs  of  .venous  stasis  other 
than  slight  oedema.  As  a  matter  of  fact  this  oedema  is  due  to  mal- 
nutrition rather  than  to  stasis. 

Diagnosis. — The  diagnosis  is  likewise  obscured  by  the  signs 
of  the  primary  disease.  It  rests  on  the  determination  by  percus- 
sion, or  better  by  the  fluoroscoijc,  of  marked  decrease  in  the  size 
of  the  heart,  together  with  evidence  of  prolonged  and  extreme 
emaciation. 

Prognosis. — The  prognosis  is  that  of  the  general  cachexia, 
and  yet  a  wasted  lieart  may  become  so  feeble  as  to  cause  death. 

Treatment. — The  treatment  is  that  of  the  primary  disorder, 
since  it  can  do  but  little  good  to  administer  heart-tonics. 

IV.   SEGMENTATION  AND   FRAGMENTATION   OF  THE 
MYOCARDIUM 

The  precise  nature  of  this  condition  has  been,  and  still  is,  a 
matter  of  dispute.  Opinion  is  still  unsettled  as  regards  its  causa- 
tion, the  time  of  its  occurrence,  whether  prior  to  or  during  the 
death  agony,  and  consequently  on  the  question  whether  or  not  it 
possesses  any  practical  clinical  importance.  Renaut  first  de- 
scribed it  as  a  segmentation  of  the  heart-muscle  due  to  chemical 
and  nutritional  changes  and  assigned  to  it  definite  clinical  fea- 
tures. His  original  view  was  that  the  muscle-fibres  became  broken 
up,  segmented,  in  consequence  of  softening  of  the  cement  sub- 
stance liolding  the  cells  together.  Various  French  and  German 
writers,  notably  Przewoski  and  Klein  and  l)rowicz,  confirmed 
Renaut's  observations  and  indorsed  his  views.  Others,  chiefly 
von  Recklinghausen  and   Tedeschi,   discovered   disintegration   of 


SEGMENTATION  AND  FRAGMENTATION  OF  THE  MYOCARDIUM  669 

the  cardiac  muscle-libres,  but  declared  it  was  due  to  rupture,  i.  e., 
fragmentation  of  the  cells,  which  occurred  during  the  death  agony 
in  consequence  of  overstimulation  and  irregular  contractions. 

Although  they  found  fragmentation  in  otherwise  normal 
hearts  of  individuals  who  had  died  suddenly  by  violence  or  other- 
wise, still  in  the  majority  of  instances  it  was  in  hearts  that  showed 
chronic  fibrous  and  fatty  change,  or  the  fragmentation  was  discov- 
ered in  persons  who  had  suffered  from  acute  infections  or  lesions 
of  the  central  nervous  system.  Indeed,  Tedeschi  found  the  condi- 
tion in  48  per  cent  of  236  cases  of  death  from  all  sorts  of  causes. 
The  statements  of  von  Recklinghausen  caused  Eenaut  to  modify 
his  views  somewhat,  and  in  1804,  at  the  first  French  Congress  for 
Internal  Medicine,  he  described  the  process  as  due  to  swelling, 
"  gigantism  "  of  the  muscle-cells  and  alteration  of  the  intercon- 
tractile  plasma  which  render  the  cells  brittle  and  disposed  to 
fracture,  while  at  the  same  time  there  is  softening  of  the  cement 
that  leads  to  segmentation.  Eenaut  still  held,  therefore,  to  his 
assertion  that  the  process  constitutes  a  distinct  and  recognisable 
clinical  entity. 

Since  that  time  the  subject  has  been  discussed  by  numerous 
observers,  chiefly  in  France  and  Germany,  English  and  Ameri- 
can writers  have  had  little  or  nothing  to  say  on  the  subject,  be- 
cause, it  may  be,  of  its  being  still  sub  judice,  and  as  yet  not  be- 
lieved to  possess  practical  value  to  the  clinician.  The  only  impor- 
tant contributions  that  have,  so  far  as  I  know,  appeared  in  this 
country  at  this  present  writing,  are  by  Ludwig  Hektoen  and  John 
Bruce  MacCallum.  The  former  made  a  careful  study  of  a  large 
number  of  hearts  from  lower  animals,  both  small  and  large,  and 
from  over  100  human  beings  that  had  died  suddenly  as  a  result  of 
violence,  or  slowly  or  suddenly  in  consequence  of  a  great  variety 
of  acute  and  chronic  affections,  some  of  them  cases  of  either  in- 
dependent or  secondary  heart-disease.  Hektoen's  observations 
agreed  with  those  of  writers  on  the  Continent  as  respects  the  fre- 
quency with  which  dissociation  of  the  heart-muscle  occurs  in  both 
sexes,  at  all  ages,  in  all  sorts  of  acute  infectious  and  chronic  dis- 
eases without  associated  cardiac  lesions  and  in  hearts  manifest- 
ing the  ordinary  myocardial  degenerations,  hypertrophy  and 
atroj^hy. 

Thus,  of  190  cases  of  deaths  from  a  great  variety  of  causes 


670  DISEASES  OF   THE  HEART 

and  in  both  sexes,  lie  found  segmentation  in  G5.78  per  cent,  while 
in  10  instances  of  traumatic  and  usually  instantaneous  death  the 
condition  was  present  in  all.  Hektoen  states  that  whenever  seg- 
mentation was  present  to  any  extent  there  was  also  more  or  less 
fragmentation.  It  is  his  opinion  that  segmentation  is  due  to  a 
disproportion  between  tlie  violence  of  fibrillar  contractions  and 
the  cohesive  strength  of  the  cement  substance,  and  thinks  that  in- 
travital alterati(m  of  the  muscle-cells  may  predispose  to  cement- 
softening  and  consequent  segmentation ;  it  is  not  impossible,  there- 
fore, for  excessive  cardiac  contractions  during  excitement,  coitus, 
etc.,  to  lead  to  sudden  death  through  segmentation  of  the  myocar- 
dium. 

The  symptoms  attributed  by  Renaut  to  disintegration  of  the 
muscle-fibres  are  disordered  action  and  feeble  apex-impulse  of  the 
heart,  some  increase  in  the  area  of  cardiac  dulness,  an  uncertain 
systolic  murmur,  and  it  may  be  slight  a'dema.  These  are,  how- 
ever, not  at  all  peculiar  to  segmented  hearts,  but  are  observed  in 
hearts  that  have  undergone  other  forms  of  degeneration.  It  is 
strange,  therefore,  that  Renaut  and  his  pupils  should  consider  the 
process  susceptible  of  clinical  recognition.  I  shall  not  devote  more 
space  to  its  consideration,  but  allow  the  following  sentences,  taken 
from  Plektoen's  paper,  to  sum  up  the  whole  matter.  "  All  the 
other  authors  regard  general  and  focal  segmentation  as  an  acci- 
dental or  secondary  phenomenon  occurring  in  the  course  of 
infections  and  intoxications  in  connection  with  tlie  primary  and 
secondary  lesions  of  asystolic  hearts,  and  with  fatal  traumatism. 
It  constitutes  an  episode  in  the  course  of  the  principal  affection. 
While  it  possesses  an  anatomical  individuality,  it  is  so  common 
that  it  would  be  difficult  to  say  in  what  disease  it  would  surely 
be  absent  after,  say,  the  twentieth  year,  and  it  would  take  a  very 
long  time  to  enumerate  all  the  diseases  in  Avhicli  it  has  been  found 
present." 


CHAPTER    XXYII 

PEDUNCULATED    AND    BALL-THROMBI    OF  THE 

HEART 

Among  the  tumours  of  the  heart  may  be  included  those  rare 
formations  which  are  found  in  the  cardiac  cavities  and  are  in 
reality  thrombi.  They  differ  from  cardiac  thrombosis  (marantic) 
in  the  chronicity  of  their  development,  the  changes  they  undergo, 
and  in  their  clinical  history,  since  they  do  not  give  rise  to  emboli. 
Like  vascular  thrombi,  some  of  them  undergo  organization,  and 
when  attached  to  the  inner  surface  of  the  heart-wall  by  a  pedicle 
are  known  as  pedunculated  thrombi  or  true  polypi  of  the  heart. 

Others,  called  hall-thrombi,  have  either  become  detached  from 
their  pedicle,  or  having  been  formed  by  the  deposition  of  suc- 
cessive layers  of  fibrin  upon  a  primary  nucleus,  and  unattached, 
roll  about  free  in  the  chamber  where  they  are  formed.  Both 
varieties  are  exceedingly  rare,  but  of  the  two,  ball-thrombi  have 
been  much  less  frequently  encountered. 

At  the  Reunion  of  Russian  Physicians  at  St.  Petersburg  in 
1893,  in  honour  of  Pirogoff,  Pawlowski  reported  a  case  of  true 
heart  polypus  that  had  come  under  his  observation.  In  this  paper 
he  stated  that  diligent  research  in  the  literature  up  to  that  date 
had  enabled  him  to  collect  only  25  cases,  including  his  own.  Wil- 
liam Welch,  however,  in  his  admirable  article  on  cardiac  throm- 
bosis in  Allbutt's  System  of  Medicine,  states  that  he  has  found  8 
others  in  the  literature,  making  33  in  all.  Small  as  is  this  num- 
ber, that  of  ball-thrombi  is  still  less.  Von  Ziemssen,  in  the  report 
of  a  case  at  the  Vienna  meeting  of  the  German  Congress  for  In- 
ternal Medicine  in  1890,  stated  that  he  had  been  able  to  collect 
only  4  cases  besides  his  own.  His  research  for  published  cases 
had  been  superficial,  however,  for  Welch  mentions  4  cases,  with  a 
reference  to  a  fifth,  that  had  been  reported  in  England  prior  even 
to  von  Recklinghausen's,  which  by  German  authors  was  consid- 

671 


672  DISEASES   OF   THE   HEART 

ered  the  earliest  recorded.  Since  von  Ziemssen's  there  have  been 
others  reported,  so  that  uj)  to  date  there  have  been  20  published 
instances  of  ball-throHd)i.  Sonic  oi  these  I  had  myself  discovered 
in  the  literatniic  before  I  had  the  good  fortune  to  peruse  Welch's 
article.  The  others  have  been  taken  from  Welch's  list.  The  en- 
tire number  will  be  found  at  the  close  of  this  chapter. 

Pedunculated  thrombi  may  be  found  in  any  of  the  cardiac 
cavities  excepting  the  right  ventricle,  although  by  far  most  fre- 
quently in  the  left  auricle.  Twenty-five  were  in  this  cavity,  4  in 
the  right  auricle,  and  a  like  number  in  the  left  ventricle.  The 
point  of  attachment  is  various,  although  the  interauricular  sa^p- 
tum  seems  to  be  the  most  frequent  seat  of  the  polypi,  near  the 
foramen  ovale.  Of  Pawlowski's  list  of  cases,  12  arose  from  the 
sseptum,  5  being  from  the  fossa  ovalis.  Two,  including  Paw- 
lowski's, were  attached  to  the  posterior  wall  of  the  left  auricle, 
2  within  the  appendix,  and  1  to  the  mitral  valve.  In  the  other 
cases  the  precise  point  of  attachment  is  not  stated.  In  size  and 
form  the  polypi  diifer,  being  likened  to  a  pear,  a  small  heart,  a 
cone,  a  bullet,  a  walnut,  and  a  hen's  egg,  the  average  comparison 
being  to  a  walnijt. 

The  pedicle  is  generally  compact  and  strong,  and  in  most 
cases  the  polyp  is  covered  by  a  thin  membrane  thought  to  be  an 
extension  of  the  endocardium  (Pawlowski).  He  also  states  that, 
according  to  Wilkinson  King,  some  polypi  could  be  injected 
through  the  coronary  vessels,  while  in  others  this  did  not  succeed. 
In  some  of  the  r(>corded  cases  the  tumours  contained  calcareous 
deposits,  others  were  cystic.  In  all  instances  of  these  heart- 
thrombi  there  is  disease,  usually  narrowing,  at  the  auriculo-ven- 
tricular  orifice  or  some  other  condition,  as  dilatation,  that  has  led 
to  stagnation  of  the  blood  in  the  cardiac  cavity  containing  the 
tumour.  In  Pawlowski's  case  there  was  mitral  stenosis  of  an 
extreme  degree. 

Von  Ziemssen  states  that  ImlJ-thromhi  are  for  the  most  part 
of  the  size  of  a  walnut,  spherical,  smooth,  with  no  rounded  cor- 
ners, and  showing  no  trace  of  a  pedicle.  In  liis  case  the  mass  was 
beautifully  round  and  smooth,  as  if  turned  by  machinery,  and  ex- 
hibited numerous  indentations  upon  its  surface.  The  thrombus 
was  firm,  and  ii))oii  being  sliced  into  sections  sliowcd  successive 
layers  of  fibrin-f<jnnatioii.     In  the  ccnti-o  was  a  small  mass  that 


PEDUNCULATED  AND   BALL-THROMBI   OF   THE   HEART     673 

had  evidently  served  as  the  basis  upon  which  the  fibrin  had  been 
deposited.  Running  up  through  the  thrombus  in  radiating  lines 
towards  the  circumference  were  delicate  fibrous  bands,  which  ter- 
minated each  in  a  depression  on  the  surface,  and  appeared  by 
their  organization  and  contraction  to  have  occasioned  the  super- 
ficial indentations.  The  mitral  orifice  was  also  greatly  stenosed  in 
von  Ziemssen's  case.  It  may  be  remarked  in  passing  that  in 
his  paper  von  Ziemssen  alludes  to  his  having  had  two  other  cases 
of  pedunculated  heart-thrombi,  but  Pawlowski  does  not  include 
them  in  his  list,  and  I  have  not  discovered  where  they  were  pub- 
lished. 

In  Wood's  case  the  ball  measured  1^  inch  in  diameter,  was  of  a 
dark-red  colour,  and  made  up  of  an  outer  wall  ^  of  an  inch  thick, 
comjjosed  of  a  large  number  of  fibrinous  laminae  and  containing 
a  mass  of  coagulated  blood.  The  feature  in  this  case,  considered 
by  Welch  as  unique,  was  that  "  adherent  to  the  wall  of  the  auri- 
cle, near  the  mitral  valve,  was  a  firm,  oval  thrombus  on  the  free 
surface  of  which  was  a  superficial  concavity  which  formed  a 
"  kind  of  socket  for  the  loose  ball  to  roll  in." 

In  one  of  Legg's  cases,  that  of  a  woman  brought  into  the  hos- 
pital dead,  two  loose  balls  were  discovered  in  the  left  auricle.  In 
Osier's  second  case  Welch  states  that  an  ovoid  thrombus,  resem- 
bling in  size  and  shape  a  thick  chestnut,  was  found  with  its 
smaller  end  sticking  in  the  moderately  narrowed  funnel-shaped 
mitral  orifice,  from  which  it  was  readily  removed.  "  At  one 
pole  of  the  thrombus  was  an  irregular  roughened  spot  indicating 
a  former  attachment,  probably  to  a  thrombus  in  the  appendix." 

In  Arnold's  case  the  ball-thrombus  was  elastic,  as  if  composed 
of  fluid  incased  by  a  thin  membrane.  At  one  spot  the  surface 
was  roughened  and  of  a  speckled  appearance,  as  if  at  this  point  it 
had  once  been  in  contact  with  the  wall,  while  close  by  was  a 
short  thread-like  prolongation  which  might  have  served  as  its 
means  of  attachment.  The  endocardium  of  the  auricle  was  smooth 
and  of  normal  appearance.  The  appendix  was  filled  by  a  throm- 
bus, broken  down  at  its  centre,  and  attached  by  a  ribbon-like  ex- 
tremity to  the  internal  aspect  of  the  tip  of  the  appendix.  This 
mass  projected  into  the  cavity  of  the  auricle.  It  is  reasonable  to 
infer,  therefore,  that  these  two  thrombi  were  originally  one,  a 
small  fragment  having  become  detached  and  ultimately  converted 
44 


G74  DISEASES   OF   THE   HEART 

into  the  ball.  The  mitral  oriiice  was  the  seat  of  obstructive 
disease. 

In  Redtenbaeher's  case  there  was  a  funnel-shaped  mitral  ori- 
fice and  valve  that  barely  admitted  the  tip  of  one  linger.  In  the 
greatly  dilated  auricle  were  two  thrombi,  one  a  ball  3.5  centi- 
metres in  diameter,  round,  and  even  in  contour,  of  a  brownish-red 
colour,  and  covered  with  fine  fibrous  threads,  soft  and  elastic ;  the 
other  a  long  mass,  which  was  attached  inside  the  ajipendix  by  a 
pedicle,  extended  into  the  auricle. 

From  the  very  meagre  description  I  have  been  able  to  find  of 
Stange's  case,  it  appears  that  a  thrombus  was  found  free  in  the 
interior  of  the  left  auricle,  which  thrombus  was  described  as  flat- 
tened {ahgeplaftetcn).  The  mitral  valves  were  slightly  insutfi- 
eient,  and  there  was  evidence  of  old  aortic  valvular  disease.  It 
may  be  questioned,  therefore,  if  this  case  can  be  properly  classi- 
fied with  von  Ziemssen's  and  the  others,  since  they  all  showed  more 
or  less  stenosis  of  the  auriculo-ventricular  ring,  and  von  Ziemssen 
expressly  states  that  in  typical  instances  mitral  narrowing  is 
present. 

Ewart  and  Kolleston  have  described  a  cardiac  thrombus  which 
was  discovered  at  the  necropsy  in  a  forty-three-year-old  female. 
It  was  hour-glass  in  form,  attached  to  the  lower  back  part  of  the 
foramen  ovale,  and  projected  through  the  mitral  orifice  into  the 
cavity  of  the  left  ventricle,  but  without  disease  of  the  ring  or 
valve.  The  clot  was  old  at  its  centre,  with  fresh  fibrin  deposits  on 
its  surface.  The  patient  had  had  some  chest  trouble,  probably 
pleuro-])neinii(tnia,  in  February,  189G,  and  afterward  a  systolic 
apex-murmur  with  a  snapping  first  sound ;  subsequently  a  pre- 
systolic bruit  developed,  and  she  died  with  symptoms  of  failing- 
circulation  from  mitral  disease. 

This  interesting  case  a])pears  to  Ix^  unique,  since  the  orifice 
was  not  iiarr()W('<l. 

Pathogenesis  and  Etiology. — Two  theories  arc  offered  to 
explain  the  formation  of  pedunculated  heart-thromhi.  One  is 
that  they  are  due  to  the  coagulation  of  blood  in  the  dilated  cavity 
in  consequence  of  the  retardation  of  the  stream  incident  to  the 
obstruction  at  the  auriculo-ventricnlar  orifice.  To  this  must  also 
l)e  added,  aceoi-djng  to  von  Kcckliiighausen's  view  of  thrombosis 
in  genci'al,  an  ethlyiiig  or  wliirliug  motion  of  the  blood.      These 


PEDUNCULATED   AND   BALL-TIIROMBI   OF   THE   HEART      075 

thrombi  become  attached  to  the  wall,  and  subsequently  undergo 
organization. 

The  other  explanation  is  the  one  advanced  by  Bostroem,  and 
accepted  by  both  Welch  and  Eomberg  as  applicable  to  some  of  the 
cardiac  polypi  at  least.  This  is  that  true  heart-polypi  are  throm- 
bosed varices  of  small  veins  in  the  interauricular  sicptum  or  result 
from  haemorrhages  into  the  sa?ptum.  This  view  is  based  on  Bos- 
troem's  examination  of  two  such  polypi,  one  of  which  he  showed  to 
be  a  thrombosed  varix,  the  other,  which  filled  the  right  auricle,  to 
be  the  result  of  hemorrhage  into  the  wall.  "  Therefore,"  says 
Welch,  "  it  would  appear  that  the  nature  of  these  formations  is  not 
always  the  same."  It  is  this  difference  in  the  nature  of  heart- 
polypi  which  has  led  to  the  diversity  of  opinion  concerning  their 
origin. 

Ball-thromhi  are  without  doubt  true  heart-clots  which  may  have 
been  formed  by  the  deposition  of  successive  layers  of  fibrin  prob- 
ably upon  a  central  nucleus  or  matrix.  The  question  that  does  not 
appear  to  have  been  settled  in  respect  to  every  reported  case  is 
whether  they  were  formed  as  detached  masses,  or  were  originally 
parts  of  an  attached  coagulum,  from  which  they  had  become 
broken  off.  Some  of  the  balls  have  presented  roughened  spots 
and  tiny  rudimentary  pedicles,  which  seemed  to  make  it  reason- 
ably certain  that  they  were  once  attached  to  thrombi  discovered  in 
the  appendix.  The  smooth  rounded  form  appears,  as  suggested 
by  von  Recklinghausen,  to  have  been  caused  by  their  rolling 
about  in  the  blood-stream. 

ISTeither  sex  is  exempt,  yet  women  are  more  frequently  be- 
fallen than  are  males,  probably  for  the  reason  that  they  furnish 
a  larger  contingent  of  examples  of  mitral  stenosis.  Polypi  have 
been  found  in  the  young  and  the  old,  yet,  singularly  enough,  Paw- 
lowski's  list  fails  to  comprise  any  case  between  the  ages  of  twenty 
and  thirty,  a  circumstance  which  he  thinks  may  be  utilized  in 
arriving  at  a  diagnosis.  As  regards  ball-thrombi,  however,  there 
are  several  cases  which  were  observed  in  persons  of  an  age  falling 
in  this  third  decade  of  life.  Finally,  there  must  be  a  constrictive 
valvular  disease  to  lead  to  stasis  and  coagulation  of  the  blood. 

Symptoms. — Whether  the  tumour  is  a  pedunculated  polypus 
or  a  ball-thrombus,  the  symptoms  are  such  as  characterize  an  ex- 
treme degree  of  circulatory  embarrassment  arising  from  stenosis 


676  DISEASES  OF  THE   HEART 

of  one  or  the  other  auriciilo-ventriciilar  orifice,  generally  the  left. 
The  patients  usually  suffer  nuich  from  dyspnoea,  even  while  at 
rest,  the  difficulty  often  assuming  a  paroxysmal  or  asthmatic  type. 
Cough  is  present  in  most  instances,  and  cyanosis  is  a  noticeable 
feature.  There  is  severe  congestion  of  all  the  viscera,  scanty  albu- 
minous urine,  and  opdema  of  the  lower  extremities,  it  may  be  of 
the  serous  cavities.  The  pulse  may  or  may  not  be  accelerated,  but 
it  is  always  strikingly  small  and  feeble.  Indeed,  the  scanty  filling 
of  the  arterial  system  evinced  by  the  pulse,  and  the  exaggerated 
cono-cstion  in  the  veins,  are  features  commented  on  by  all  observ- 
ers.  The  almost  total  obliteration  of  the  pulse  is  far  in  excess  of 
what  is  observed  even  in  high  grades  of  mitral  stenosis.  In 
rhythm  the  pulse  is  not  peculiar,  since  it  may  be  irregular,  inter- 
mittent, or  unchanged. 

A  very  striking  symptom,  which  von  Zicmssen  lays  stress  upon 
as  having  been  present  in  all  three  of  his  cases,  was  gangrene  of  a 
circumscribed  area  on  the  foot,  associated  with  oedema  and  a  truly 
cadaveric  coldness  of  the  extremities :  phenomena  due,  in  his  opin- 
ion, not  to  embolism,  but  to  arterial  thrombosis.  This  results 
from  the  very  deficient  filling  of  the  aortic  system  and  sluggish 
flow  in  the  arteries  of  the  lower  extremities. 

In  Pawlowski's  case  the  patient,  a  female  aged  forty-seven,  a 
school-teacher,  the  fatal  illness  lasted  five  wrecks,  and  was  char- 
acterized by  an  intermittent  pyrexia,  which  at  first  gave  rise  to 
the  diagnosis  of  typhoid.  Great  circulatory  embarrassment  and 
a  mitral  murmur  did  not  at  first  attract  attention,  and  indeed 
were  variable,  particularly  the  presystolic  murmur.  At  the  au- 
topsy there  was  found  in  addition  to  the  polypus  and  mitral  ob- 
struction a  splenic  tumour  due  to  infarcts  in  its  centre.  These 
were  broken  down  and  purulent,  and  probably  accounted  for  the 
septic  fever. 

One  of  Hertz's  patients,  a  woman  of  thirty-nine,  was  admitted 
in  a  state  of  advanced  cardiac  feebleness  and  consequent  circula- 
tory embarrassment,  and  in  spite  of  treatment  died  at  the  end  of 
forty-eight  hours,  Arnold's  patient  was  a  servant-girl  of  twenty- 
three  who  entered  the  hospital  witli  all  appearances  of  some  bron- 
chial or  pneumonic  affecti(m.  A  mitral  lesion  was  discovered. 
Death  took  place  four  weeks  after  admission. 

In  Proust's  case  the  patient  was  a  man  of  fifty-eight  who  was 


PEDUNCULATED   AND   BALL-TIIROMBI   OF   THE   HEART     677 

ill  five  inontlis  with  most  distrcssiiiii,'  symptoms  of  oml)arrassod 
circulation,  l)rcathlessness,  vertigo,  cold  sweats,  and  absence  of 
pulse  that  were  thought  to  depend  upon  mitral  disease  and  secon- 
dary failure  of  the  right  ventricle.  Death  was  the  result  of 
asphyxia.  The  necropsy  disclosed  a  pedunculated  thrombus  in 
the  right  auricle  3  inches  in  length  and  attached  to  the  sseptum. 

It  is  thus  seen  that,  however  great  may  be  the  differences  in 
the  duration  of  the  symptoms,  these  all  evince  a  similarity  in  the 
manifestations  of  valvular  obstruction  of  an  extreme  degree. 

As  regards  the  physical  signs,  these  may  be  said  to  be  those  of 
a  stenosis  of  an  auriculo-ventricular  orifice,  usually  the  left.  It 
must  be  remarked,  however,  that  the  characteristic  presystolic 
murmur  is  not  always  present.  Indeed,  von  Ziemssen  states  that 
after  the  thrombus  has  formed  and  begun  to  produce  symptoms, 
the  diastolic-presystolic  murmur  which  previously  existed  may 
disappear.  A  very  suggestive  character  of  the  murmur  in  such 
a  case  is  its  intermittency,  coming  and  going,  audible  upon  one 
examination  and  absent  at  another.  This  must  depend  in  some 
way  upon  the  presence  of  the  mass,  at  one  time  the  flow  being 
sufiiciently  forcible  to  generate  a  bruit,  at  another  too  languid 
and  small  to  produce  sonorous  vibrations. 

Diagnosis. — This  is  obviously  a  matter  of  great  difficulty 
if  not  of  actual  impossibility.  So  far  as  I  can  learn,  an  intra- 
vitam  diagnosis  has  not  been  recorded.  The  existence  of  the 
thrombus  must  always  be  a  matter  of  conjecture  rather  than  cer- 
tainty. However,  if  in  a  case  of  apparent  mitral  disease,  or 
indeed  of  cardiac  feebleness  from  any  other  cause,  the  embar- 
rassment in  the  circulation  be  greater  than  seems  accounted  for 
by  the  lesion  discovered,  if  localized  gangrene  of  the  foot  occurs 
in  a  case  of  mitral  disease,  and  evidently  not  due  to  arteriosclero- 
sis or  embolism,  and  lastly  if  a  presystolic  or  other  murmur  comes 
and  goes  in  an  unaccountable  fashion,  one  may  entertain  the  sus- 
picion of -a  heart-thrombus.  One  cannot  from  these  data  diagnose 
it  with  certainty. 

Von  Ziemssen  considers  three  conditions  indispensable  to  an 
intra-vitam  diagnosis  of  an  autochthonous  cardiac  thrombus:  (1) 
There  must  be  the  physical  signs  of  a  mitral  stenosis,  since  this 
lesion  was  present  in  all  the  typical  cases  on  record.  The  evidence 
of  this  valvular  defect  must  have  been  found  at  a  time  prior  to 


678  DISEASES   OF  THE   HEART 

the  formation  of  the  tlu'oinbiis,  however,  because  the  niuriiiur 
characteristic  of  stenosis  disappears  after  the  symptoms  of  throm- 
bosis make  their  appearance.  (2)  Manifestations  of  an  obstruc- 
tive lesion  of  the  left  heart  are  not  only  indispensable,  but  they 
must  be  present  to  a  degree  not  seen  in  simple  stenosis.  These 
are  orthopncea,  cyanosis,  coldness  of  the  extremities,  but,  above  all, 
extraordinary  smallness  and  feebleness  of  the  arterial  circulation 
as  evinced  by  the  pulse.  (3)  The  circumscribed  gangrene  of  the 
foot  which  was  present  in  all  of  his  and  one  of  Hertz's  cases. 
With  regard  to  this  symptom,  however,  Redtenbacher  calls  atten- 
tion to  the  fact  of  its  absence  in  his  case,  although  expressly  stat- 
ing that  had  the  patient's  life  been  sufficiently  prolonged  he  be- 
lieves it  would  have  eventually  resulted,  such  was  the  feeble- 
ness of  the  ])ulse. 

Prognosis. — This  is  absolutely  unfavourable,  since  the  de- 
gree of  obstruction  to  the  circulation  is  incompatible  with  recov- 
ery of  the  patient  or  even  with  a  tolerable  existence  after  symp- 
toms have  once  declared  themselves.  The  exact  mode  of  death  is 
a  matter  of  discussion.  Hertz  thought  the  ball-thrombus  acted  as 
a  ball-valve  and  occasioned  a  total  arrest  of  circulation  by  being 
driven  into  the  orifice  by  the  blood-current.  Von  Recklinghausen 
showed  this  to  be  unlikely,  owing  to  the  anatomical  character  of 
the  stenosed  opening.  This  is  apt  to  present  not  a  funnel-like  cav- 
ity into  which  the  ball  might  be  pressed,  but  is  a  shallow  depres- 
sion of  a  transversely  elliptical  form  so  smooth  as  to  favour  the 
mass  being  rolled  off  again  after  once  resting  against  the  greatly 
contracted  mitral  opening.  It  is  this  supposed  action  present  in 
Osier's  case  which  has  led  to  the  appellation  of  "  ball-valve " 
sometimes  given  to  the  condition.  Death  is  likely  to  supervene, 
therefore,  through  strangulation  or  in  consequence  of  cardiac  or 
general  asthenia,  or  through  some  of  the  iiinncdiate  causes  of 
dissolution,  such  as  occur  in  severe  valvular  disease,  or  by  reason 
of  complications  on  the  side  of  the  lungs  and  general  system. 
The  fatal  result  is  usually  preceded  by  a  longer  or  shorter  period 
of  suffering,  and  yet  in  Ilartell's  case  the  patient,  a  farmer  aged 
fifty-nine,  ate  breakfast  apparently  in  usual  health,  went  to  the 
field  to  work,  and  was  found  dead  three  quarters  of  an  hour  later. 

Treatment. — This  is  purely  sym])f()iii;i1i('.  Nothing  can  be 
done  to  remove  the  thrombus,  even  if  its  i)resence  can  be  diagnos- 


PEDUNCULATED   AND  *BATjL-TnROMBI   OF   THE   HEART      Cud 


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680  DISEASES  OF   THE   HEART 

ticated.  The  associated  valve-lesion  will  cause  death  eventually, 
and  we  can  do  no  more  than  ameliorate  the  patient's  distress. 
Indeed,  we  may  deem  ourselves  fortunate  if  we  can  accomplish 
this. 

Bibliography  of  Cases  of  Ball-Thrombi 

Arnold.      Bcitriige  zur  pathologisclien  Anatoniie  und  zur  iillgemcincn  Patho- 

logie,  Jena,  1890. 
BosTROEM.     Deutsches  Archiv  fur  klin.  Med.,  1895,  Iv,  p.  219. 
EwART.     Trans.  Clin.  Soc,  London,  1896-97,  xxx,  p.  190. 
IlARTiLL.     Brit.  Med.  Jour.,  May  22,  1886,  p.  973. 
Hertz.     Deutsches  Archiv  flir  klin.  Med.,  Bd.  xxxvii,  S.  74. 
OsLER.     Johns  Hopkins  Hospital  Reports,  1890,  ii,  p.  56.     Montreal  Med.  Jour., 

1897,  XXV,  p.  729. 
Pawlowski.     Zeitschrift  fur  klin.  Med.,  1894,  xxvi,  p.  482.- 
Proust.     Conipte  rendu  d.  .sc.  med.  et  do  l)iologie,  1864,  i,  p.  41. 
Recklinghausen,  von.     Handbuch  dcr  allg.  Path,  des  Kreislaufs  u.  d.  Ernah- 

rung,  1883,  p.  131. 
Redtenbacher.     Wien.  klin.  Wocli.,  1892,  v,  p.  689. 
RoLLESTON.     Lancet,  1897,  vi,  p.  1546. 

Stance.     Arb.  a.  d.  path.  Inst,  in  Gtittingen,  Berlin,  1893,  S.  232-234. 
Welch.     Allbutt's  System  of  Medicine. 
Wood.     Edinburgh  Med.  and  Surg.  Jour.,  1814,  x,  p.  50. 
Ziemssen,  von.     Vortrag  gehaltcn  auf  dem  IX.  Congresse  fiir  inneren  Med.  in 

Wien,  1890,  S.  281. 


CHAPTER    XXVIII 

DEXTROCARDIA 

This  term  signifies  a  transposition  of  the  heart  into  the  right 
side  of  the  thorax.  This  condition  may  be  congenital  or  acquired. 
Most  congenital  displacements  of  the  heart  occasionally  met  with 
possess  interest  chiefly  for  the  pathologist.  The  organ  may  be 
situated  in  the  cervical  region,  within  the  abdominal  cavity  or 
upon  the  exterior  of  the  chest  (ectopia  cordis). 

CONGENITAL  DEXTROCARDIA 

This  form  is  the  most  frequent  of  all  displacements  and  is  of 
clinical  as  well  as  pathological  interest,  inasmuch  as  the  physi- 
cian may  be  called  on  to  determine  whether  the  displacement  is 
pathological  or  normal  to  the  individual  concerned,  and  therefore 
devoid  of  danger.  In  most  instances  this  abnormal  situation  of 
the  heart  is  associated  with  transposition  of  the  other  viscera,  a 
condition  which  has  received  the  name  situs  viscerum  inversus. 
That  this  is  not  invariable  has  been  noticed  by  Breschet. 

The  displaced  heart  occupies  the  same  relative  position  on  the 
right  side  as  it  does  normally  at  the  left,  while  the  stomach  and 
spleen  are  in  the  right  and  the  liver  in  the  left  hypochondrium. 
The  position  of  the  intestines  is  also  reversed,  so  that  the  rectum 
lies  in  the  right  instead  of  in  the  left  iliac  fossa. 

Symptoms. — Congenital  dextrocardia  occasions  no  symp- 
toms unless  it  be  associated  with  other  cardiac  anomalies,  as  some- 
times is  the  case.  It  is  stated,  however,  that  patients  with  this 
displacement  of  the  heart  are  apt  to  develop  pulmonary  tubercu- 
losis. Apropos  of  this  possibility  I  recall  the  case  of  a  Miss  A., 
who  applied  to  me  for  an  examination  because  she  had  had  her 
attention  directed  to  the  fact  that  her  heart  pulsated  upon  her 
right  side,  and  she  desired  to  learn  if  it  possessed  any  special  im- 

681 


682  DISEASES  OF   THE   HEART 

portance.  Examination  showed  the  apex-shock  was  in  the  fifth 
right  interspace,  about  1  inch  inside  the  vertical  nipple-line.  Car- 
diac dnlness  was  of  normal  extent,  and  beginning  a  finger's 
breadth  to  the  left  of  the  sternnm,  reached  nearly  to  the  right 
mamillary  line.  The  heart-sounds  were  of  normal  strength  and 
clearness,  and  were  situated  at  the  right  of  the  sternum.  Per- 
cussion of  the  abdomen  showed  gastric  tympany  beneath  the  right 
costal  arcli  and  hepatic  dnlness  in  the  left  hypochondrium.  At 
that  time  the  patient  was  in  perfect  health  and  gave  no  history  of 
tuberculosis  in  the  family.  Yet  before  two  years  had  elapsed  she 
developed  pulmonary  tuberculosis,  to  which  she  succumbed  about 
a  year  later. 

Diagnosis. — The  detection  of  the  dextrocardia  depends  upon 
the  recognition  of  the  cardiac  impidse,  dnlness,  and  sounds  to  the 
right  of  the  median  line  and  their  absence  at  the  left.  Its  congeni- 
tal nature  is  shown  by  the  transposition  of  the  abdominal  viscera, 
which  can  scarcely  be  a  matter  of  difficulty  of  determination. 

ACQUIRED   DEXTROCARDIA 

Morbid  Anatomy. — This  form  of  dextrocardia  may  be 
complete,  the  heart  lying  entirely  within  the  right  half  of  the 
thorax,  or  it  may  be  partial,  in  which  case  the  organ  is  situated 
mainly  but  not  wholly  to  the  right  of  the  median  line.  As  this 
transposition  of  the  heart  is  a  pathological  condition,  the  other 
viscera  remain  in  their  customary  position.  The  morbid  anatom- 
ical appearances  in  these  cases  are  found  chiefly  in  the  lungs  and 
their  investing  membranes,  since  the  heart  is  not  necessarily  the 
seat  of  any  other  disease  than  that  incident  to  the  torsion  of  its 
supports. 

The  organ  is  fixed  at  its  base  by  the  great  vessels,  and  cannot 
become  displaced  in  either  direction  without  undergoing  more  or 
less  rotation  upon  its  long  axis.  In  dextrocardia  there  must  be 
twisting  of  the  arteries  and  veins  at  its  l)ase,  aud  hence  authors 
have  speculated  on  the  direction  in  which  the  heart  must  turn  to 
admit  of  displacement  to  the  right.  Sibson  maintained  that  the 
heart  rotates  in  such  manner  as  to  bring  the  left  ventricle  to  the 
front  and  flic  riglit  chambers  to  the  rcai-,  wliilc  von  Schroetter 
argued  tbat  the  right  ventricle  turns  towards  llie  left  so  that  the 
left  ventricle  recedes  still  further  into  the  background. 


DEXTROCARDIA  683 

A  inomeut's  reflection  will  ('onvinco  one,  however,  tliat  the 
direction  in  which  the  heart  rotates  is  determined  hy  the  displace- 
ment and  twisting  of  its  sn})ports  or  by  the  point  of  attachment  of 
adhesions  and  the  angle  in  which  they  pull.  In  a  paper  on  dex- 
trocardia, contributed  by  me  in  1888,  this  question  was  fully  dis- 
cussed, and  I  there  reported  2  cases  which  proved  conclusively 
that  the  heart  may  rotate  in  either  direction,  so  that  both  Sibson 
and  von  Schroetter  were  right.  (For  details  see  Medical  jSTews, 
1884-1888.) 

The  twisting  and  strain  to  which  the  aorta  and  pulmonary 
artery  are  subjected  may  exert  a  detrimental  effect  on  the  heart. 
Thus  in  the  case  of  a  child  which  I  reported  the  aorta  was  found 
constricted  by  the  superior  vena  cava,  which  was  stretched  tightly 
across  it,  and  the  narrowing  of  the  aorta  thus  occasioned  had  led 
to  dilatation  of  the  left  ventricle.  It  is  possible,  therefore,  for  this 
abnormal  and  constrained  position  of  the  heart  to  lead  to  its 
hypertrophy  and  dilatation  and  to  constriction  as  well  as  stretch- 
ing of  the  large  vessels  at  its  base. 

Etiology. — This  is  found  in  pathological  processes  that  exert 
either  pressure  or  traction  upon  the  heart.  The  former  is  brought 
about  through  the  accumulation  in  the  left  pleural  cavity  of  air 
(pneumothorax)  or  of  liquids  (pleuritis  with  effusion  and  empy- 
ema). With  the  absorption  or  artificial  removal  of  the  exuda- 
tion the  heart  usually  returns  to  its  normal  situation,  but 
the  formation  of  pleuritic  adhesions  and  obliteration  of  the  left 
pleural  sac  may  serve  to  maintain  the  organ  in  its  acquired  loca- 
tion. The  pressure  exerted  may  be  sufficient  to  push  the  heart 
entirely  beyond  the  median  line,  so  that  its  apex  strikes  the  chest- 
wall  outside  the  right  mamillary  line,  and  Walshe  says  this  may 
take  place  wdthin  thirty-six  hours.  Ordinarily  the  organ  is  not 
greatly  displaced,  and  the  apex  may  come  to  lie  at  any  point 
between  the  midsternal  line  and  the  right  nipple. 

When  the  heart  is  drawn  over  into  the  right  side,  it  is  through 
the  traction  exerted  by  pleuro-pericardial  adhesions  acting  in  con- 
junction with  more  or  less  cirrhosis  of  the  right  lung.  This  was 
the  cause  in  all  three  of  my  cases.  The  primary  cause  may  be  a 
trauma,  or  tuberculosis  of  the  lung  may  be  the  initial  etiological 
factor.  Whatever  be  the  predisposing  cause,  the  pleuritic  adhe- 
sions undergo  contraction  slowlv,   and   a  considerable  length  of 


684  DISEASES   OP  THE   HEART 

time  must  elapse  before  the  dextrocardia  is  completed.  In  this 
class  of  cases,  moreover,  are  seen  the  most  extreme  examples  of 
cardiac  transposition,  the  heart  assuming  a  nearly  horizontal  posi- 
tion in  its  new  situation.  It  lies,  of  course,  under  these  condi- 
tions, immediately  beneath  the  anterior  chest-wall  and  is  uncov- 
ered by  hmir. 

Symptoms. — These  may  consist  of  those  phenomena  ordi- 
narily associated  with  venous  stasis — i.  e.,  cyanosis,  dyspnoea,  fee- 
bleness and  rapidity  of  the  pulse,  palpitation,  and  after  a  time 
oedema,  scantiness  of  the  urine^  and  other  evidences  of  visceral 
congestion,  or  the  clinical  picture  may  be  rather  that  of  the  pul- 
monary aifection  with  or  without  symptoms .  of  cardiac  insuffi- 
ciency. The  symptoms  may  be  of  a  severe  type  throughout,  but 
more  frequently  the  course  of  the  disease  is  protracted,  and  the 
symptoms  are  mild,  depending  upon  the  nature  of  the  associated 
pulmonary  aifection.  In  a  word,  there  is  nothing  distinctive  of 
the  clinical  history  of  these  cases  unless  it  be  their  chronicity. 

Diagnosis. — The  detection  of  the  fact  of  the  dextrocardia 
can  hardly  be  a  matter  of  difficulty,  particularly  in  cases  in  which  it 
is  associated  with  or  dependent  upon  chronic  disease  of  the  right 
lung.  When  due  to  accumulaticm  of  air  or  liquid  in  the  left  pleu- 
ral cavity  with  compensatory  emphysema  of  the  right  lung,  the 
condition  may  escape  the  detection  of  the  careless  observer.  It  is 
conceivable  also  that  an  aneurysm  pulsating  low  down  and  to  the 
right  of  the  sternum,  or  a  pulsating  empyema  between  the  ster- 
num and  right  nipple,  might  mislead  the  inexperienced  or  super- 
ficial examiner.  The  history  of  the  case  and  careful  exploration 
of  the  chest  ought,  however,  to  protect  against  so  gross  an  error. 

Inspection  and  Palpation. — These  disclose  pulsation  in  the 
region  of  the  right  nipple  and  its  absence  in  its  usual  situation. 

Percussion. — This  reveals  an  area  of  absolute  and  relative 
dulness  to  the  right  of  the  sternum  having  the  characteristic  out- 
line of  the  heart,  while  a  similar  area  of  dulness  is  absent  on  the 
left.  Unlike  congenital  cases,  percussion  discloses  gastric  tym- 
pany and  hepatic  dulness  in  their  normal  position. 

Auscultation. — This  enables  one  to  perceive  that,  instead  of 
the  heart-sounds  being  audible  in  their  normal  situation,  they  are 
heard  at  the  right  of  the  median  line. 

The  physical  signs,  by  wliicli  are  recognised  the  i)ulmonary 


DEXTROCARDIA  685 

diseases  that  bring  about  an  acquired  dextrocardia,  do  not  need 
to  be  here  stated. 

If  occasionally  cardiac  murmurs  are  heard  in  this  class  of 
cases,  it  is  not  always  easy  to  determine  whether  they  are  organic 
from  valvular  disease,  or  are  accidental  and  due  in  some  way  to 
the  alterations  in  the  cardiac  walls  and  large  vessels  incident  to  the 
rotation  of  the  organ.  The  history  of  cases  of  acquired  dextro- 
cardia shows  that  accidental  bruits  are  not  uncommon.  For  the 
differentiation  of  the  murmurs  one  must  rely  on  the  rules  that 
have  been  stated  already  in  the  introductory  chapter. 

Prognosis. — In  most  instances  this  may  be  said  to  be  that 
of  the  lung  condition,  and  yet  in  a  case  of  complete  acquired  dex- 
trocardia with  presumably  considerable  torsion  of  the  vessels,  the 
condition  is  likely  to  shorten  the  prospect  of  the  patient's  life. 
Nevertheless,  one  of  my  patients  was  alive  and  in  ordinary 
health  fourteen  years  after  my  first  examination.  The  prognosis 
in  each  case  depends  upon  the  evidence  or  not  of  cardiac  feeble- 
ness and  disordered  circulation,  all  of  which  signs  have  been  suffi- 
ciently set  forth  in  previous  chapters. 

Treatment. — This  must  be  based  on  the  indications  of  each 
case  and  the  principles  that  apply  to  other  forms  of  cardiac  in- 
adequacy. It  is  needless  to  remark  that  nothing  can  be  done  for 
the  relief  of  the  dextrocardia  in  those  instances  in  which  it  is 
owing  to  traction  from  permanent  disease  within  the  right  half 
of  the  thorax. 


CHAPTEK    XXIX 
CONGENITAL    DISEASES    OF  THE    HEART 

Some  of  these  possess  a  pathological  rather  than  a  clinical  in- 
terest, since  they  render  extra-iiterinc  existence  impossible.  For  a 
detailed  description  of  snch  the  reader  is  referred  to  works  on 
pathology,  (^jngenital  cardiac  aifections  were  the  object  of  much 
interest  and  even  of  superstition  in  the  early  days  of  anatomic 
investigation.  It  is  to  Meckel,  Bonilland,  Rokitansky,  Dorsch, 
Peacock,  Knssniaul,  and  Lcbcrt  that  the  profession  is  chiefly  in- 
debted for  a  scientific  elucidation  of  their  various  modes  of  de- 
velopment. 

Morbid  Anatomy. — Of  the  congenital  defects  of  the  heart 
that  are  the  result  of  developmental  errors,  the  most  frequently 
found  and  at  the  same  time  the  least  important  clinicall}^,  is  an 
increase  in  the  number  of  cusps  in  the  semilunar  valves  of  the 
aorta  or  })ulmonary  artery.  This  condition  is  more  frequent  at 
the  pulmonary  than  at  the  aortic  opening.  Four  and  even  five 
segments  have  been  found.  The  supernumerary  cusps  are  usu- 
ally smaller  than  the  others,  but  the  ring  may  be  equally  divided 
between  the  increased  nimiber  of  segments.  The  presence  of  a 
diminished  number  is  of  less  frequent  occurrence.  Two  cusps 
have  then  become  united,  leaving  no  trace  of  the  line  of  union, 
or  at  best  a  very  slight  one.  According  to  Osier,  this  condition 
is  more  common  at  the  aortic  orifice,  but  two  of  his  twenty-one 
instances  having  occurred  at  the  pulmonary.  Osier  further  states 
that  this  defect  is  an  important  one,  as  the  conjoined  cusjis  are 
very  a))t  to  nndergo  sclerotic  changes. 

Stenosis  of  the  puhnonary  or  aortic  orifices  may  result  from 
the  more  or  less  complete  fusion  of  all  three  cusps  (Fig.  78),  and 
this  may  even  ])roceed  to  complete  atresia.  The  fusion  may  be 
the  result  of  fcr-tal  endocarditis  or  developmontMl  error.  In  the 
former  case  the  valve  ])resents  mnch  the  same  ai)poarancc  as  after 
686 


CONGENITAL   DISEASES   OF   THE   HEART 


687 


postnatal  endocarditis.  Vegetations  may  cover  the  cusps,  project 
into  tlie  ventricle,  or  fill  the  sinuses  of  Valsalva.  At  other  times, 
however,  the  nnited  valves  may  present  no  signs  of  endocarditis, 
being  combined  to  form  a  funnel,  which  may  show  signs  of  very 
slight  sclerosis.  Stenosis  or  atresia  of  the  auriculo-ventricular 
orifices  is  of  much  less  frequent  occurrence  than  of  the  arterial 
openings.  In  either  case  the  congenital  disease  is  more  frequent 
on  the  right  side  on  account  of  the  more  frequent  location  of  foetal 
endocarditis  on  that  side.  Pott  says  that  for  one  congenital  aortic 
defect  there  are  twenty-five  pulmonary  and  tricuspid. 


Fig.  105. — Perforate  Interventricular  Septum. 


Pulmonary  stenosis,  already  considered  in  a  special  chapter,  is 
a  by  no  means  infrequent  congenital  anomaly.  Aortic  obstruction 
is  far  less  frequently  congenital.     In  either  case  if  the  obstruction 


688  DISEASES   OF  THE   HEART 

arises  earlier  than  the  eighth  week  of  foetal  life,  it  leads  to  an 
imperfect  formation  of  the  interventricular  sa^i:)tum.  This  is  due 
to  the  inequality  of  blood-pressure  in  the  two  ventricles  occa- 
sioned by  the  stenosis,  and  the  consequent  passage  of  a  stream  of 
blood  from  one  to  the  other  through  the  still  imperfect  septum, 
with  each  systole  of  the  ventricles.  This  stream  prevents  the 
union  of  the  two  fundaments  of  the  sa>ptum,  and  in  consequence, 
the  imperfection  is  almost  always  situated  at  the  pars  memhrana- 
cea,  or  point  where  the  two  embryonic  fundaments  fuse  (Fig. 
105).  This  is  high  up  on  the  sa^ptum  in  the  portion  separating  the 
two  coni  arteriosi. 

If  the  obstruction  be  established  later  in  embryonic  life,  the 
interventricular  sa^ptum  is  usually  found  entire,  but  the  inter- 
auricular  sa^ptum  is  usually  imperfect,  and  the  ductus  arteriosus 
open.  The  stenosis  need  not  necessarily  be  located  at  the  valve 
to  produce  these  effects,  since  narrowing  of  the  conus  on  either 
side,  the  so-called  stenosis  of  the  heart,  acts  in  the  same  way.  It 
is  not  always  possible  to  say  whether  the  imperfect  closure  of  the 
sa?ptum  preceded  the  obstruction  of  the  pulmonary  ostium  or  of 
the  conus,  or  whether  it  followed  the  other  lesion.  In  the  light  of 
Kiissmaul's  conclusions,  that  defects  of  development  predisposes 
to  endocarditis,  the  former  hypothesis  is  not  unlikely. 

Patency  of  the  foramen  ovale  results  from  any  condition 
causing  a  considerable  inequality  in  the  blood-pressure  in  the  two 
auricles  at  the  time  when  it  is  normally  closed.  This  may  be  due 
to  stenosis  of  one  or  the  other  of  the  auriculo-ventricular  orifices, 
or  obstruction  at  either  of  the  arterial  openings  may  secondarily 
influence  the  blood-pressure  in  the  auricles,  and  so  cause  persist- 
ence of  the  foramen.  The  condition  is  often  combined  with  a  de- 
fective interventricular  sa'ptuiii,  or  j)atent  ductus  arteriosus,  for 
the  reason  that  all  these  imperfections  are  due  to  the  same  cause. 
Patency  of  the  foramen  ovale,  or  rather  an  incomplete  union  of 
the  valve  with  the  ring,  is  by  no  means  always  to  be  considered 
a  pathological  condition.  According  to  Romberg,  such  a  condi- 
tion exists  in  at  least  half  of  all  cases.  This  may  not  produce 
symptoms,  however,  as  when  the  valvular  flap  is  of  suflicient  size 
the  pressure  of  the  blood  in  the  left  iiuriclc  keeps  it  closed  and 
prevents  any  interchange  of  blood. 

The  ductus  arteriosus  j)crsists  as  a  patulous  vessel,  when,  at 


CONGENITAL   DISEASES  OF  THE   HEART  689 

the  time  it  should  normally  be  obliterated,  the  blood-pressure  in 
the  aorta  and  pulmonary  artery  is  so  unequal  that  a  current  flows 
through  the  ductus  from  one  to  the  other.  Thus  in  a  case  of  pul- 
monary stenosis  developing  early  in  f(jotal  life,  the  contents  of  the 
right  ventricle,  experiencing  difficulty  in  passing  through  the  pul- 
monary orifice,  enter  the  left  chamber  through  the  imperfect  in- 
terventricular sfcptum,  and  only  a  diminished  quantity  of  blood 
passes  into  the  pulmonary  artery. 

On  the  other  hand,  the  aorta  receives  an  increased  amount  of 
blood  on  account  of  the  extra  supply  to  the  left  ventricle  from 
the  right  chamber  through  the  imperfect  sffiptum.  Thus  the  ten- 
sion in  the  aorta  is  rendered  higher  than  that  in  the  pulmo- 
nary artery,  and  a  portion  of  blood  passes  into  the  latter  vessel 
through  the  ductus  Botalli.  The  stream  in  the  ductus,  it  is 
to  be  noted,  is  in  this  case  flowing  in  a  direction  opposite  to 
that  normal  in  foetal  life,  which  is  from  the  pulmonary  artery 
into  the  aorta. 

Persistence  of  the  ductus  may  depend  on  aortic  as  well  as 
pulmonary  defect,  and  may  be  due  to  a  congenital  reduction  of 
the  calibre  of  the  vessel,  as  in  Fig.  lOY.  The  extreme  case  of 
atresia  of  either  artery  necessitates  the  patency  of  the  ductus  for 
the  carrying  on  of  the  circulation. 

Etiology. — There  has  been  much  speculation  upon  the  de- 
termining factors  in  the  development  of  congenital  affections  of 
the  heart.  Foetal  endocarditis  is  quite  generally  attributed  to  the 
agency  of  infectious  diseases  operating  through  the  maternal  circu- 
lation. It  has  not  been  at  all  clear  what  influences  lead  to  the  pro- 
duction of  developmental  anomalies.  Some  have  sought  to  ac- 
count for  these  in  tendency  or  inclination  to  perversion  of  growth 
impressed  upon  the  germ  by  the  parent,  and  hence  regard  such 
abnormalities  as  stigmata  of  degeneracy.*  This  hypothesis  is 
based  largely  on  the  fact  that  developmental  defects  of  other  parts 
of  the  body  are  not  infrequently  associated  with  congenital  car- 
diac anomalies.     Others,  again,  hold  that  these  abnormalities,  de- 

*  F.  Simpson,  in  4,253  autopsies  of  the  insane,  found  fenestration  of  the  aortic 
valve  75  times;  of  the  right  semilunar,  18;  of  the  mitral,  6;  and  of  the  tricuspid, 
2.  It  was  especially  frequent  in  men.  Supernumerary  and  rudimentary  valves 
were  found  very  often.  It  would  be  interesting  to  ]<now  how  these  findings  would 
compare  with  those  from  the  same  number  of  necropsies  of  the  sane. 
45 


690  DISEASES  OF  THE  HEART 

velopmental  as  well  as  endocarditic,  are  the  result  of  pathogenic 
agencies,  the  differences  in  result  being  determined  by  the  period 
of  fa'tal  life  at  which  these  agencies  work.  This  conclusion  ap- 
pears justified  by  the  results  of  Fere's  experiments. 

This  investigator  found  that  if  eggs  in  the  stage  of  incubation 
were  inoculated  at  a  sufficiently  early  period  with  pathogenic  or- 
ganisms or  their  toxins  errors  of  development  resulted.  This  is 
certainly  a  very  satisfactory  explanation,  and  is  one  that  accords 
with  our  modern  notions  of  the  bacterial  origin  of  most  maladies. 
It  is  more  reasonable  also  than  the  assumption  that  defects  in  the 
septa  are  secondary  to  an  inflammatory  process  that  was  limited 
to  the  orifice  aifected,  since,  as  pertinently  suggested  by  Osier, 
it  is  difficult  to  understand  how  an  inflammation  could  fail  to 
attack  the  whole  heart  at  a  time  when  the  icetns  and  heart  are  so 
diminutive. 

The  reason  for  the  predominance  of  endocarditis  in  the  right 
as  compared  with  the  left  heart  in  utero  is  probably  to  be  found 
in  the  greater  blood-pressure  within  the  right  chambers.  After 
birth  has  altered  the  course  of  the  blood-stream  by  calling  into  use 
the  vessels  of  the  pulmonic  system,  blood-pressure  becomes  higher 
in  the  left  heart,  and  this  half  now  becomes  relatively  more  liable 
to  inflammatory  processes. 

Symptoms. — The  disorders  now  under  consideration  do  not 
possess  individuality  as  regards  their  clinical  features.  Patency 
of  the  foramen  ovale  even  when  of  considerable  size  does  not  nec- 
essarily preckule  the  possibility  of  long  life  and  may  not  give 
rise  to  symptoms.  Duroziez,  cited  by  Gibson,  discovered  such  a 
condition  in  a  woman  who  died  of  erysipelas  at  the  age  of  sev- 
enty-six. 

Wlieii  not  dependent  upou  ])ulnionary  stenosis  or  other  valvu- 
lar defect  there  may  even  be  an  absence  of  uiurnnir  or  other  ob- 
jective evidence  of  the  patency. 

A  defect  in  the  interventricular  saeptum  may  also  fail  to 
manifest  itself  by  sul)jective  symptoms,  and  there  may  not  te 
even  cyanosis,  which,  as  we  shall  see  later  on,  is  ordinarily  one  of 
the  commonest  and  most  significant  features  of  congenital  heart- 
disease. 

Stenr»sis  or  atresia  of  the  pulmonary  orifice  or  artery,  on  the 
other  hand,  rarely  fails  to  occasion  grave  circulatory  embarrass- 


CONGENITAL   D'ISEASES  OF  THE   HEART  691 

ment,  and  hence  well-marked  subjective  and  objective  symptoms. 
It  is  in  this  the  most  frequently  recognised  congenital  affection, 
therefore,  especially  when  attended  by  sseptum  imperfections,  that 


Fig.  lOij. — Shows  the  Cyanosis  of  Congenital  Heabt  Disease,  the  Drum-Stick  Fingee- 
Tips,  the  Bulging  Pr^cordia,  and  the  Distention  of  the  Abdomen  ln  its  Upper 
Zone  due  to  Hepatic  Congestion. 

patients  complain  of  symptoms.    It  is  worthy  of  note  in  this  con- 
nection, however,  that  my  patient,  whose  case  was  narrated  in  the 


692  DISEASES  OF  THE  HEART 

chapter  on  Pulmonary  Stenosis,  denied  having  suffered  any  incon- 
venience from  his  cardiac  lesion,  although  this  was  pronounced, 
and  indeed  was  not  aware  of  its  existence  until  informed  of  it  by 
myself.  Even  up  to  the  last  his  symptoms  were  chiefly  attributa- 
ble to  the  tuberculosis  of  the  lungs,  which  was  secondary  to  his 
valvular  disease. 

Children  who  are  born  with  serious  disorders  of  the  heart 
evince  notable  backwardness  of  development,  both  mental  as  well 
as  bodily.  Their  intellectual  processes  are  sluggish,  and  they 
learn  to  talk  at  a  later  age  than  do  normal  children.  In  stature 
they  are  iisually  stunted,  even  dwarfish,  and  they  are  apt  to  pre- 
sent certain  striking  peculiarities  in  appearance.  The  nostrils 
and  lips  are  thick  and  protruding,  and  the  chest  is  more  or  less 
deformed  in  consequence  of  bulging  of  the  pnvcordia.  There  is 
marked  clubbing  of  the  fingers  and  toes  with  incurvation  of  the 
nails,  so  that  by  German  authors  they  are  likened  to  drum-sticks 
(Trommelschlaeger). 

The  most  cliaracteristic  feature,  however,  in  persons  with  con- 
genital cardiac  afTections  is  cyanosis.  This  morbus  cceruleus  of 
old  authors  is  a  general  but  not  uniform  blueness  of  the  skin 
and  mucous  membranes,  which  is  sometimes  of  so  deep  a  hue  as 
to  be  actually  purple.  It  is  most  intense  in  those  parts  that  are 
naturally  red — the  lips,  nostrils,  ears,  cheeks,  nails,  elbows,  and 
knees.  It  is  always  intensified  by  exertion  and  during  the  act 
of  coughing. 

The  cyanosis  and  other  visible  circulatory  effects  of  congenital 
cardiac  disease  is  well  exhibited  in  Fig.  106,  which  is  the  copy 
of  a  photograph  taken  of  a  nine-year-old  girl  whom,  through  the 
courtesy  of  Drs.  Houston  and  Breid,  T  had  the  privilege  of  seeing 
at  the  Maurice  Porter  Hospital  for  Children.  The  little  patient 
had  been  a  blue  haby  from  birth,  and  was  brought  to  the  hospital 
on  account  of  attacks  of  pra'cordial  ])ain  during  which  slie  moaned 
continuously  and  displayed  signs  of  great  cardiac  feebleness.  I 
saw  her  in  one  of  these  attacks  and  noted  tlie  following:  L^niform 
bluish  hue  of  the  surface,  exce})ting  the  lips  and  ends  of  the  fin- 
gers, which  were  of  a  deep  purple  tint;  pronounced  emaciation  of 
the  extremities,  with  exquisitely  bulbous  terminal  phalanges;  pro- 
nounced prominence  of  the  cardiac  area  and  distention  of  the 
hepatic  region  as  far  as  the  umbilicus ;  turgescence  of  the  external 


CONGENITAL   DISEASES  OP  THE   HEART  693 

jugulars;  rapid  and  extremely  thready  pulse;  epigastric  pulsa- 
tion, but  no  a'dcnia. 

Superficial  cardiac  dulness  was  greatly  increased  in  all  direc- 
tions, and  deep-seated  dulness  was  of  a  quadrangular  outline, 
reaching  from  the  second  costal  cartilage  to  the  seventh  in  the 
median  line,  and  from  2  inches  outside  of  right  sternal  margin 
nearly  to  the  left  anterior  axillary  line.  Its  great  breadth  at  its 
upper  part  over  the  auricles  was  especially  noticeable.  The  heart- 
sounds  were  very  feeble,  and  over  the  body  of  the  heart  was  a 
scarcely  audible  yet  apparently  systolic  murmur.  When,  however, 
a  hypodermic  injection  of  ^.  of  a  grain  of  morphine,  given  to  re- 
lieve the  patient's  distress,  had  stimulated  the  heart  and  enabled 
it  to  partially  empty  its  overdistended  chambers,  and  the  little  suf- 
ferer had  grown  quiet,  the  bruit  came  out  loud  and  distinct.  It  was 
then  found  to  have  its  maximum  intensity  in  the  third  left  inter- 
space, close  to  the  sternum,  and  to  possess  a  very  short  presystolic 
portion. 

Erom  the  great  dilatation  of  the  auricles,  the  position  and 
character  of  the  murmur  and  evident  signs  of  impeded  venous  cir- 
culation, it  was  thought  likely  that  this  was  a  case  of  patent  fora- 
men ovale,  or  other  sseptum  defect,  but  whether  or  not  with  any 
other  lesion  could  not  be  determined.  The  congenital  nature  of 
the  defect  was  attested  by  the  plus  percentage  of  haemoglobin, 
which  was  115  per  cent,  and  the  number  of  red  cells,  which  were 
in  the  neighbourhood  of  7,000,000. 

It  is  needless  to  remark  that  cyanosis  is  not  limited  only  to 
congenital  heart-lesions,  since  it  is  also  present  at  times,  in  ac- 
quired cardiac  disease.  In  the  latter  cases,  however,  it  is  never  so 
intense. 

Many  attempts  have  been  made  to  explain  the  occurrence  of 
cyanosis,  but  as  yet  none  is  generally  accepted  as  quite  satisfac- 
tory. It  has  been  attributed  to  venous  stasis  and  to  deficient 
oxygenation  of  the  blood,  and  apropos  of  this  theory  it  is  stated  by 
Vierordt  that  Moritz  found  the  CO2  increase  to  between  45  and 
46  per  cent.  Romberg  thinks  the  cyanosis  may  be  attributed  to 
the  abnormal  admixture  of  arterial  and  venous  blood.  The  in- 
tensity of  its  hue  is  due  to  the  dilatation  of  the  capillaries  (Vie- 
rordt), which  takes  place  to  a.  far  greater  extent  than  can  be  the 
case  in  those  diseases  in  which  stasis  develops  more  rapidly. 


694  DISEASES  OF   THE   HEART 

Striking  as  is  tlie  tint  of  the  integument,  there  are  certain 
other  changes  in  the  blood  that  are  still  more  remarkable.  Toe- 
uiessen  first  announced  that  in  cyanosis,  examination  of  the  blood 
shows  an  increase  in  its  specific  gravity  and  its  corpuscular  in- 
gredients. His  observations  have  been  abundantly  confirmed  by 
niimerous  investigators.  The  specific  gravity  in  a  boy  of  ten 
years  was  found  by  Banholzer  to  be  1071.8,  while  the  hiemo- 
globin  was  100,  the  red  cells  9,447,000.  The  white  corpuscles  have 
been  ropoatedly  ascertained  to  be  as  high  as  16,000.  In  a  case 
of  congenital  defect  recently  observed  by  me,  hannoglobin  was 
115;  total  red  cells  per  centimetre  7,120,000;  total  white  cells 
per  centimetre  10,400. 

Xo  theory  to  explain  this  peculiarity  of  the  blood  is  gener- 
ally acce])ted.  Malasscz  appears  to  have  demonstrated  that  the 
blood  of  the  superficial  parts  contains  a  greater  number  of  red 
cells  than  docs  that  of  the  deeper  parts,  and  accordingly  Penzoldt 
concludes  this  difference  is  due  to  an  evaporation  of  fluids  at  the 
surface.  This  theory  of  a  thickening  of  the  blood,  which  Rom- 
berg mentions  as  having  been  established  by  Krehl,  is  objected  to 
by  Gibson,  and  I  think  justly,  on  the  ground  that  the  volume  of 
the  blood  would  have  to  be  reduced  at  least  a  half  in  those  cases  in 
which  the  number  of  red  corpuscles  is  doubled. 

It  has  also  been  claimed  that  this  augmentation  in  the  num- 
ber of  coloured  corpuscles  is  a  compensatory  process  on  the  part 
of  nature  in  order  thereby  to  supply  more  oxygen  to  the  tissues, 
and  also  provide  a  more  adequate  means  of  having  the  COg  re- 
moved, (libson's  liy])othesis  is  so  ingenious  that  it  is  here  quoted 
at  length.  '^  In  venous  stasis  the  corpuscles  are  insufiiciently  oxy- 
genated, they  cannot  thoroughly  perform  their  duties  as  oxygen 
carriers,  and  they  cannot  yield  so  much  oxygen  to  the  tissues.  It 
must  liii'tlicr  he  rciiicinbcrcd  that  in  cyanosis  thei-e  is  less  metabo- 
lism of  the  tissues,  and  theiefore  less  waste  ])rodu(!ed.  hi  a  word, 
the  functions  of  the  cor))uscles  being  lessened,  the  tear  and  wear 
which  they  undergo  is  rccluced,  and  the  duration  of  their  indi- 
vidual existence  increased.  The  number  of  the  corpuscles  must 
in  this  way  be  proportionately  augnumted,  and  this  must  lead  to 
the  numericiil  increase,  as  well  as  to  the  high  percentage  of  ha>mo- 
giobin,  until  a  l)alancc  is  struck  between  tlic  production  and  de- 
struction (d'  the  bl(jod-corpuscles." 


CONGENITAL  DISEASES  OF  THE  HEART  695 

In  contrast  to  the  usual  results  of  blood  examinations  in  these 
cases  Mouille  is  cited  by  Vierordt  as  having  found  a  reduction, 
the  red  cells  ranging  between  3,500,000  and  4,500,000,  yet  this 
in  no  way  invalidates  the  general  proposition  that  the  corpuscu- 
lar elements  are  increased  in  cyanosis.  Finally,  it  should  be 
stated  that  a  similar  though  less  striking  increase  is  observable  in 
cyanosis  in  acquired  heart  disorders. 

Laennec  and  Rokitansky  attributed  to  cyanosis  a  protective 
influence  against  the  development  of  pulmonary  tuberculosis. 
Their  views  are  erroneous,  however,  since  it  is  a  well-known  fact, 
as  has  been  stated  in  the  chapter  on  Pulmonary  Stenosis,  that 
patients  with  this  affection,  in  which  cyanosis  is  particularly 
apt  to  occur,  are  especially  prone  to  tuberculous  disease  of  the 
lungs. 

Another  symptom  in  cases  of  cyanosis  is  coldness  of  the  skin, 
particularly  of  the  extremities,  and  hence  these  patients  are  re- 
markably sensitive  to  cool  atmospheres.  They  are  also  very  sub- 
ject to  dyspnoea  and  often  manifest  pronounced  shortness  of 
breath  on  comparatively  trifling  exertion,  as  was  present  in  my 
case ;  but  this,  as  we  have  seen,  is  a  symptom  common  to  all  forms 
of  cardiac  disease  in  the  stage  of  defective  compensation.  In 
these  cases,  when  dyspnoea  is  a  marked  feature,  there  is  usually 
evidence  of  considerable  visceral  stasis.  In  congenital  cases,  on 
the  contrary,  breathlessness  is  not  infrequently  pronounced  out  of 
all  proportion  to  the  signs  of  engorgement  in  the  various  organs, 
aside  from  the  capillary  dilatation  emphasized  by  Vierordt. 

This  lack  of  such  venous  stasis  as  would  ordinarily  be  ex- 
pected in  cardiac  disorders  of  such  evident  gravity,  is  attributed 
by  Romberg  to  the  slowness  with  which  the  veins  have  been  re- 
quired to  accommodate  themselves  to  their  abnormal  burden 
(uebetiastung) .  Nevertheless,  the  deficient  arterial  blood-supply 
and  the  sluggish  return  of  venous  blood  and  the  defective  metab- 
olism lead  to  disturbances  of  function  on  the  part  of  the  various 
viscera  rriore  or  less  severe  and  commensurate  with  heart-power. 
The  variations  in  the  pulse  will  be  spoken  of  in  connection  with 
the  physical  signs  now  to  be  considered. 

Physical  Signs. — Ins'pection. — This  is  of  special  value 
only  in  the  cases  in  which  there  are  cyanosis,  a  dwarfish  appear- 
ance, clubbing  of  the  fingers,  praecordial  bulging,  and  other  signs 


696  DISEASES   OF  THE   HEART 

of  a  long-standing  circulatory  embarrassment.  In  such  a  case, 
moreover,  there  is  nsnally  the  history  that  the  patient  "  was  a  bine 
baby."  Scrutiny  of  the  cardiac  area  may  detect  displacement  of 
the  apex  indicative  of  hypertrophy,  but  in  all  this  there  is  noth- 
ing to  attest  the  exact  nature  of  the  lesion.  In  not  severe  cases  of 
congenital  disease,  as  persistence  of  the  ductus  or  patency  of  the 
foramen  ovale,  there  may  be  nothing  whatever  in  the  j)atient's 
aspect  to  suggest  the  existence  of  cardiac  mischief. 

Palpation. — Of  the  serious  congenital  defects  which  come  to  a 
clinical  recognition  stenosis  of  the  pulmonary  orifice  or  conus  is 
by  far  the  most  frequent,  and  it  is  in  this  affection  that  palpation 
is  of  special  value.  This  usually  detects  a  systolic  thrill  in  the 
second  and  third  left  intercostal  spaces  close  to  the  sternum.  This 
may  be  so  soft  and  weak  as  to  be  scarcely  percejitible,  or  so  coarse 
and  strong  as  to  tickle  the  hand.  In  patency  of  the  foramen,  of 
the  duct,  or  even  of  the  interventricular  saeptum,  there  may  be  no 
thrill  unless  associated  with  some  obstructive  lesion,  as  just  men- 
tioned. 

For  the  most  part  authors  pay  but  little  attention  to  the  pulse, 
since  it  is  thought  to  possess  no  distinctive  characters.  It  should, 
however,  be  given  particular  study  in  cases  of  pulmonary  steno- 
sis, since,  according  to  Starck  and  Renvers,  its  volume  assists  in 
determining  the  question  whether  or  not  there  is  closure  of  the 
interventricular  sa'ptum.  If  the  Sieptum  is  perfect  the  supply  of 
blood  to  the  left  heart  is  diminished,  and  hence  the  pulses  of  the 
upper  extremities  are  small.  When,  on  the  contrary,  communica- 
tion exists  between  the  ventricles,  a  side  channel  is  provided  by 
which  the  left  ventricle  receives  a  large  supply  of  blood,  and  hence 
the  pulses  are  of  greater  volume.  Consequently,  if  in  a  given 
case  of  pulmonary  constriction  the  pulse  shows  a  degree  of 
strength  and  volume  out  of  proportion  to  what  would  be  naturally 
expected,  it  suggests  the  likelihood  of  incomplete  closure  of  one  or 
both  of  the  septa. 

Kolisko  is  reported  to  have  stated  that  when  persistence  of 
Botalli's  duct  exists  secondary  to  atresia  or  great  narrowing  of 
the  isthmus  of  the  aorta  or  to  congenital  stenosis  of  its  ostium,  the 
pulses  in  the  lower  extremities  are  larger  tliau  tliose  in  the  upper. 
This  is  due  to  the  fact  that  the  arteries  given  off  from  the  aortic 
arch  receive  an  abnormally  small  volume  of  blood,  whereas  a  por- 


CONGENITAL   DISEASES   OF  THE    HEART  697 

tion  of  the  blood  pent  up  in  the  puhnonary  artery  and  intended 
for  the  ascending-  aorta  through  the  left  ventricle  is  switched  off 
through  the  patent  duct  and  enters  the  descending  aorta,  thus 
supplying  the  lower  extremities  with  a  disproportionate  share  of 
blood. 

Percussion. — As  in  acquired  heart-disease  this  means  of  in- 
vestigation should  not  be  neglected,  since  it  is  of  extreme  impor- 
tance to  discover  possible  modifications  of  cardiac  dulness.  In 
pulmonary  obstruction  the  absolute  and  relative  dulness  are  both 
increased  to  the  right  and  downward  in  consequence  of  the  right- 
ventricle  hypertrophy.  In  patent  foramen  ovale  and  a  defective 
ventricular  sseptum  the  cardiac  outline  may  or  may  not  be  in- 
creased transversely,  according  to  the  severity  of  the  lesion. 
When  the  ventricular  sii'ptum  is  incomplete  the  greater  blood- 
jDressure  in  the  left  ventricle  forces  a  portion  of  the  contents 
through  into  the  cavity  of  the  right  ventricle.  This  chamber  be- 
comes surcharged,  and  tends  therefore  to  hypertrophy  and  dilata- 
tion, which  condition  is  shown  by  increase  of  cardiac  dulness  in 
that  direction.  Nevertheless,  in  both  patency  of  the  S£eptum  and 
foramen  unassociated  with  other  lesions  prsecordial  dulness  may 
in  some  cases  remain  normal. 

Auscultation. — This  usually  furnishes  the  most  valuable  in- 
formation concerning  the  presence  and  nature  of  these  congenital 
affections  by  the  detection  of  a  murmur.  Yet  in  cases  of  sseptum 
defects,  including  of  course  the  foramen,  there  may  be  no  mur- 
mur of  any  kind.  When  such  a  bruit  exists,  it  is  usually  a  loud 
systolic  murmur  heard  throughout  the  cardiac  area,  particularly 
over  the  base.  It  does  not  appear  to  be  limited  to  any  area,  as 
are  the  murmurs  of  acquired  valvular  disease ;  and  this  fact,  when 
noted,  possesses  a  certain  amount  of  value. 

Robert  Maguire  thinks  that  the  systolic  bruit  of  a  defective 
ventricular  saeptum  is  most  distinct  over  the  situation  of  the  inter- 
ventricular groove,  and  decreases  in  intensity  as  the  stethoscope 
recedes  from  this  line  in  either  direction.  As,  however,  the  only 
case  he  has  reported,  so  far  as  I  have  been  able  to  learn,  has  not 
yet  come  to  a  necropsy,  the  proof  of  his  contention  is  wanting, 
and  although  the  statement  may  appear  plausible,  it  cannot  yet  be 
accepted  unreservedly. 

Worcester  has  reported  a  case  of  patency  of  the  foramen  ovale, 


698  DISEASES  OF  THE   HEART 

toe-ether  witli  a  small  defect  in  the  interventricular  Sicptimi  just 
below  the  right  semilunar  vahes,  which  was  discovered  post  mor- 
tem in  a  negro  of  fifty-seven  who  died  of  general  paralysis.  Sev- 
eral years  before  there  was  detected  a  long  loud  systolic  murmur 
audible  over  the  entire  chest.  The  absence  of  symptoms  during 
life  is  to  be  inferred  from  the  fact  that  he  served  as  a  soldier 
during  the  civil  Avar.  The  heart  was  found  only  moderately 
hypertrophied.  There  is  nothing,  therefore,  distinctive  of  the  mur- 
mur of  foramen  or  ventricular  sa'ptum  patency.  Cabot  speaks 
of  the  quality  of  the  bruit  as  harsh  and  vibrant;  but  there  is  in 
this  statement  nothing  at  all  distinctive.  In  the  case  of  a  boy 
recently  seen  by  me  there  was  a  loud  systolic  murmur  not  trace- 
able to  any  particular  ostium. 

For  a  description  of  the  murmur  of  pulmonary  stenosis,  as 
well  as  the  other  signs,  the  reader  is  referred  to  the  chapter  on 
that  subject. 

The  auscultatory  phenomena  due  to  persistence  of  Botalli's 
duct  are  best  described  in  the  narration  of  a  case  I  had  under 
observation  for  several  years,  and  which  finally  came  to  necropsy. 
The  patient  was  an  undersized  woman  of  twenty-one  who  suffered 
from  breathlessness  upon  rapid  walking  and  an  uncomfortable 
pounding  of  the  heart.  Her  mother  reported  her  as  having  been 
a  small  delicate  baby,  but  as  not  having  shown  cyanosis  even  dur- 
ing fits  of  crying.  Her  only  illness  had  been  scarlatina  at  the 
age  of  nine.  The  radial  pulses  were  small,  regular,  equal,  and 
in  rate  between  90  and  100.  There  was  no  cyanosis  or  venous 
turgescence.  The  pra?cordium  was  prominent,  particularly  at  the 
left  of  the  sternum,  but  was  not  pigeon-breasted.  The  apex-beat 
was  in  the  sixth  left  interspace,  2  inches  from  the  sternum,  strong 
and  diffused. 

There  was  a  soft,  not  very  distinct  thrill  in  the  second  and 
third  left  interspaces  close  to  the  sternum,  which  was  not  syn- 
chronous with  either  systole  or  diastole,  but  was  most  pronounced 
at  the  end  of  expiration  and  beginning  of  inspiration.  It  seemed 
to  follow  the  apex-shock  by  a  very  brief  instant,  and  to  run  into 
the  long  pause.  Absolute  cardiac  diihicss  was  but  slightly  in- 
creased, whereas  the  relative  appeared  rather  too  broad.  The 
heart-sounds  were  feeble  and  obscured  l)y  ;i  loud  harsh  murmur 
that  seemed  to  be  systolic  and  audible  throughout  the  entire  prae- 


CONGENITAL   DISEASES  OF  THE   HEART 


699 


cordia,  but  most  plainly  at  the  base,  and  , was  transmitted  to  the 
lower  angle  of  the  left  scapula. 

Upon  closer  observation  it  was  perceived  that  at  the  site  of 
the  thrill  the  murmur  became  a  continuous  remitting  roar,  having 


Fig.  107. — IIkakt  from  Case  on  p.  «y8,  shovvinu    Cuncentkic    IIvpertuophv    uf    Left 
\'kntricle  and  Sound  passed  through  Patent  Ductus  Arteriosus. 


its  maximum  intensity  just  after  the  first  sound  and  its  minimum 
towards  the  end  of  the  long  silence,  but  never  entirely  ceasing. 


700  DISEASES  OF   THE   HEART 

Everywhere  the  quality  of  the  bruit  seemed  to  be  the  same.  The 
lungs,  abdomen,  and  urine  were  negative,  but  the  blood  examina- 
tion showed  a  pronounced  reduction  in  the  percentage  of  hsemo- 
globin. 

The  precise  nature  of  this  lesion  was  not  clear,  but  was  evi- 
dently congenital.  In  time,  however,  the  affection  was  decided  to 
be  either  patency  of  the  foramen  or  of  the  ductus  arteriosus.  As 
compensation  appeared  threatened,  appropriate  treatment  was  in- 
stituted, and  soon  a  satisfactory  degree  of  hypertrophy  became  re- 
established. 

To  make  a  long  story  short,  this  patient  ultimately  married 
and  was  delivered  of  a  child,  passing  through  both  pregnancy 
and  labour  without  special  difficulty.  Unfortunately  she  became 
infected  through  the  carelessness  of  her  nurse,  and  died  of  sep- 
ticoemia  in  the  second  week  of  her  puerperium. 

The  necropsy  was  made  by  Dr.  W.  A.  Evans,  who  found  foci 
of  suppuration  in  the  right  kidney  and  liver,  but  no  evidence  of 
inflannnation  in  the  cardiac  structures.  The  specimen  is  pre- 
sented in  Fig.  107.  The  left  ventricle  was  concentrically  hyper- 
trophied,  its  wall  measuring  22  millimetres.  The  wall  of  the  right 
ventricle  measured  11  millimetres,  and  was  therefore  also  thicker 
than  normal.  Both  septa  were  complete  and  the  foramen  was  not 
patent.  All  four  sets  of  valves  were  healthy,  but  the  aortic  orifice 
was  so  small  as  to  barely  admit  the  index  finger.  This  was  found, 
however,  to  correspond  in  size  to  the  lumen  of  the  artery,  whieli 
was  abnormally  narrow  throughout.  The  circmuference  of  the 
aortic  ring  was  43  millimetres ;  of  the  aorta,  just  central  to 
branches,  45  millimetres ;  at  opening  of  ductus,  43  millimetres ; 
and  6  centimetres  beyond,  40  millimetres.  Of  pulmonary  ring, 
55  millimetres;  and  of  pulmonary  artery,  55  millimetres. 

The  ductus  was  patulous,  and  u])on  searching  for  the  cause 
of  this  persistence  it  was  found  that,  instead  of  the  isthmus  being 
constricted,  or  the  aortic  arch  smaller  than  the  portion  of  the 
artery  below  the  origin  of  the  duct,  it  was  as  a  matter  of  fact  half 
a  centimetre  wider. 

In  this  case  the  narrowing  of  the  aorta  below  the  origin  of  the 
duct,  slight  as  it  was,  was  yet  sufficient  to  cause  a  portion  of  the 
blood-wave  to  be  diverted  into  the  duct  and  through  it  into  the 
])ulmonary  artery,  thus  giving  rise  to  the  ninnnnr  and  thrill.     The 


CONGENITAL   DISEASES  OF  THE   HEART  TOl 

left-ventricle  hypertrophy  was  secondary  to  the  aortic  narrowing. 
This  was  an  instance  of  chlorosis  aortica,  and  accounted  for  the 
fact  that  treatment  had  never  been  able  to  restore  the  haemo- 
globin to  its  normal  percentage. 

I  have  under  observation  at  the  present  time  two  other  pa- 
tients, one  a  woman,  the  other  a  young  man,  who  present  almost 
identical  physical  signs  and  who,  I  believe,  are  also  instances  of 
this  same  congenital  anomaly. 

Diagnosis. — As  there  are  several  affections  embraced  by 
the  term  Congenital  Cardiac  Affections,  it  would  be  wearisome 
and  unnecessary  to  recapitulate  the  physical  signs  by  which  each 
may  be  diagnosticated,  and  hence  the  reader  is  referred  to  what 
is  stated  above  under  the  caption  of  physical  signs.  It  only  needs 
to  be  here  stated  that  the  congenital  nature  of  the  affection  must 
be  determined  by  the  history  and  in  some  cases  by  a  blood  exami- 
nation. If  there  is  a  history  of  the  individual  having  been  "  a 
blue  baby  "  or  of  his  having  been  feeble  from  birth  with  evi- 
dence of  circulatory  embarrassment  directly  after  birth,  and  if 
the  child's  appearance  corresponds  more  or  less  to  that  described 
under  inspection,  there  is  strong  likelihood  of  the  cardiac  dis- 
ease being  congenital.  In  many  instances  the  parents  are  able  to 
state  that  the  family  doctor  discovered  signs  of  heart-disease  as 
soon  as  the  infant  was  born  or  in  its  earliest  weeks  of  life. 

If  the  person  presents  well-marked  cyanosis,  and  if  exami- 
nation of  the  blood  discloses  the  changes  previously  described — 
i.  e.,  an  increase  of  haemoglobin  and  red  corpuscles  over  the  nor- 
mal— the  diagnosis  of  a  congenital  defect  can  be  positively  made. 
In  some  cases,  as  of  pulmonary  stenosis,  there  may  be  nothing  to 
prove  conclusively  during  life  whether  the  disease  is  congenital 
or  acquired.  In  such  a  case,  however,  probabilities  are  always 
in  favour  of  its  prenatal  origin,  owing  to  the  great  rarity  of  the 
acquired  form. 

Finally,  in  doubtful  cases  of  persistence  of  Botalli's  duct,  it 
is  stated  that  by  means  of  the  fluoroscope  a  positive  diagnosis  may 
be  made. 

Prognosis. — As  stated  in  the  symptomatology  of  persistence 
of  the  foramen,  this  abnormality  may  occasion  no  signs  of  its  pres- 
ence, and  patients  may  reach  an  advanced  age,  and  die  of  some 
intercurrent  affection.     Unassociated  with  an  affection  of  the  pul- 


702  DISEASES  OP  THE   HEART 

moiiic  or  other  orifice,  a  defective  sreptnin  ventriciilonun  or  a  patu- 
lous ductus  arteriosus  may  also  in  no  wise  aiiect  the  prospect  of 
longevity.  It  is  far  otherwise,  however,  as  regards  pulmonary 
stenosis.  Even  when  the  patient  does  not  succumb  to  the  heart- 
lesion  directly,  he  is  most  likely  to  develop  tuberculosis  of  the 
lungs.  In  comparing  the  gravity  of  this  with  other  forms  of  con- 
genital cardiac  disease,  excepting,  of  course,  the  uncomplicated 
SiTpptum  anomalies  just  mentioned,  Komberg  states  that  up  to  the 
twelfth  year  of  life  affections  of  the  pulmonary  ostium  and  conus 
constitute  three-fifths  of  all  cases,  whereas  after  the  twelfth  year, 
owing  to  the  mortality  of  other  lesions,  these  comprise  four-fifths 
of  the  cases.  Taking  all  forms  of  congenital  cardiac  defects  to- 
gether, he  cites  Stoelker's  figures,  which,  condensed,  are  as  fol- 
lows: Out  of  79  cases  of  all  kinds,  24  died  in  the  first  six  months 
of  life,  42  had  died  before  the  end  of  the  first  year,  56  before  the 
tenth  year,  and  71  had  died  before  the  twentieth  year  of  life  was 
reached. 

It  should  be  remendjered,  moreover,  that,  according  to  Kuss- 
maid,  C(mgcnital  disorders  of  the  heart  predispose  to  endocarditis. 
In  other  respects  the  prognosis  is  influenced  favourably  or  not  by 
all  those  conditions  of  environment  that  have  been  fully  consid- 
ered in  previous  chapters.  Lastl}^,  when  compensation  has  once 
begun  to  fail  in  these  cases  there  is  small  prospect  of  much  being 
accomplished  by  treatment. 

Treatment. — As  may  be  inferred  from  the  preceding  sen- 
tence, this  must  be  largely  or  wholly  symptomatic — that  is,  in 
accordance  with  the  indications  of  each  case.  The  reader  is  re- 
ferred, therefore,  to  the  discussion  of  the  management  of  valvular 
diseases  in  general  for  the  principles  of  treatment. 


SECTION   IV 
OAEDIAC  ISTEUEOSES 

SYN. :  FUNCTIONAL  DISORDERS   OF   THE  HEART 


CHAPTER    XXX 

PALPITATION,  TACHYCARDIA,   CARDIAC    PAIN, 
PSEUDO-ANGINA    PECTORIS 

* 

Pathology. — There  is  a  class  of  disorders  which  manifest 
themselves  clinically  by  a  perverted  action  of  the  heart,  or  by 
pain  and  other  sensations  in  the  cardiac  region,  or  by  a  combina- 
tion of  the  two,  yet  in  which  no  structural  alteration  of  the  organ 
can  be  detected.  They  are  often  spoken  of,  therefore,  as  func- 
tional disorders  of  the  heart.  Objection  is  made  to  this  term  on 
the  ground  that  in  organic  cardiac  disease  there  is  a  disturbance 
of  function,  and,  strictly  speaking,  such  affections  may  also  be  des- 
ignated functional  derangements.  Furthermore,  it  cannot  be 
affirmed  absolutely  that  some  as  yet  undiscoverable  alteration  of 
the  structure  of  the  heart  does  not  underlie  or  attend  its  perver- 
sion of  function.  However  logical  such  reasoning  may  be,  the 
term  functional  has  been  sanctioned  by  usage,  and  is  generally 
understood  by  the  profession  and  the  laity  to  mean  an  affection 
which  is  not  associated  with  demonstrable  structural  lesion.  Tor 
this  very  reason  it  is  often  advisable  in  speaking  to  the  patient 
or  his  friends  to  designate  the  disturbance  as  functional.  A  fear 
or  an  exaggerated  notion  of  the  gravity  of  the  complaint  may  thus 
be  allayed.  Although  from  force  of  habit  I  frequently  speak  of 
these  affections  as  functional,  I  yet  prefer  the  designation  cardiac 
neuroses,  since  one  cannot  observe  these  cases  without  coming  to 
the  conclusion  that  the  manifestations  on  the  side  of  the  heart  are 
the  expression  of  a  disorder  of  the  nervous  system. 

.    703 


704:  DISEASES  OF   THE   HEART 

One  may  be  unable  to  detect  any  definite  pathological  lesion 
underlying  this  disturbance  of  the  nervous  nieehanisni,  and  yet  it 
cannot  be  doubted  that  some  neurosis  is  responsible  for^the  cardiac 
symptoms.  In  some  instances  the  disorder  of  the  heart's  ac- 
tion points  to  vagus  influence,  while  in  others  the  accelerator 
nerves  of  the  heart  are  responsible  for  the  manifestations.  The 
exciting  cause  may  or  may  not  be  discoverable,  but  an  attentive 
study  of  the  history  and  close  analysis  of  the  symptoms  during 
and  between  attacks  render  no  other  conclusion  tenable  than  that 
the  cardiac  and  circulatory  phenomena  are  secondary  and  sub- 
ordinate to  some  disturbance  of  the  nervous  system,  and  hence 
outside  the  cardio-vascular  apparatus. 

It  would  no  doubt  be  more  in  accord  with  the  pathology  of 
these  cases  to  relegate  these  so-called  cardiac  neuroses  to  the  do- 
main of  neurology,  wdiere  they  properly  belong ;  but  the  symptoms 
calling  attention  to  the  heart  are  so  often  the  dominant  ones  that 
they  mislead  the  patient  into  the  belief  he  has  heart-disease.  In- 
deed, the  correct  interpretation  of  the  sensations  is  often  puzzling 
to  the  physician,  and  hence  it  is  customary  to  consider  these  cases 
in  works  of  this  kind. 

Romberg  classifies  them  as  neurasthenic,  hj-sterical,  and  reflex, 
in  accordance  with  the  nervous  disorder  underlying  them.  This 
would  be  well  if  all  cases  belonged  strictly  to  these  categories,  or 
if  the  pathology  of  these  neuroses  was  clearly  understood.  Such 
is  not  the  case,  and  therefore  I  prefer  to  describe  the  various 
manifestations  without  attempting  to  divide  them  according  to 
their  apparent  etiology  into  special  groups. 

Symptoms 

Palpitation.- — Tliis  is  a  transient  derangement  of  cardiac  ac- 
tion characterized  by  an  increase  in  both  the  frequency  and  force 
of  its  contractions.  Without  warning,  the  heart  suddenly  begins 
to  beat  in  a  more  or  less  disordered  manner,  and  to  give  to  the 
individual  the  sensation  of  a  pounding  or  knocking  against  the 
ribs.  Whatever  may  be  the  variations  in  rate  and  rhythm  in  in- 
dividual cases,  it  is  this  subjective  consciousness  of  the  lieart's 
action  that  constitutes  tlie  special  cliaracteristic  of  an  attack  of 
palpitation,  and  it  appears  to  ])e  lliis  feature  wliich  alarms  the 
patient.     The  heart  may  be  rapid,  120,  130,  or  more,  or  it  may 


FUNCTIONAL  DISORDERS  705 

remain  below  100,  but  whatever  its  rate  its  action  is  violent.  In 
the  matter  of  rhythm  also  there  are  differences.  Ordinarily  the 
pulse  is  regular,  but  it  may  be  irregular  in  frequency  and  force, 
and  may  be  even  intermittent.  When  this  is  the  case  the  indi- 
vidual is  likely  to  be  thrown  into  a  state  of  great  alarm. 

Each  time  the  heart  intermits,  it  is  announced  by  a  sensa- 
tion of  the  organ  suddenly  falling  or  sinking  in  the  chest;  it  is 
often  described  as  a  "  sinking  feeling."  This  is  succeeded  the 
next  instant  by  a  powerful  throb,  a  sensation  as  if  the  heart  gave 
a  flop  or  jumped  up  into  the  throat,  and  with  this  very  uncom- 
fortable feeling  the  patient  is  apt  to  make  a  sudden  exclamation 
or  outcry,  and  perhaps  quickly  press  the  hand  against  the  pra^cor- 
dia,  as  if  trying  to  grasp  the  refractory  organ.  The  heart  may 
then  quiet  down,  or  it  may  race  off  as  madly  as  before.  It  appears 
to  me  that  in  strictly  neurotic  persons  without  any  discoverable 
organic  mischief  it  is  more  common  for  the  heart's  action  at  these 
times  to  be  rapid  and  regular  (tachycardia). 

During  the  attack  of  palpitation  there  is  often  a  violent  throb- 
bing or  pulsation  in  the  arteries  of  the  neck  or  in  the  abdominal 
aorta,  or  in  both  situations.  The  hand  placed  against  the  prse- 
cordium  readily  appreciates  the  energetic  beating  of  the  organ, 
and  not  infrequently  the  eye  perceives  a  rapid  rising  and  falling 
of  the  cardiac  region.  As  it  is  so  often  expressed  by  the  friends, 
"  you  can  see  the  heart  beat  through  the  clothes."  If  the  radial 
pulse  is  examined  during  such  an  attack  or  "  spell  with  the  heart," 
to  quote  the  popular  phrase,  it  may  be  found  full  and  quick,  or  if 
the  rate  be  extremely  rapid,  small  and  feeble.  Vaso-motor 
changes  are  also  very  apt  to  accompany  the  seizure.  The  face 
flushes  or  pales,  as  the  case  may  be,  and  the  hands  and  feet  are 
usually  cold. 

One  of  the  most  typical  examples  of  palpitation  was  presented 
in  a  young  man  who  consulted  me  only  a  few  days  ago.  He  was 
twenty-two  and  an  athlete  of  superb  physique,  standing  6  feet  2^ 
inches,  weighing  200  pounds,  and  with  muscles  of  steel.  He  is 
an  expert  boxer,  and  can  endure  an  arduous  sparring-match  with- 
out palpitation  or  shortness  of  breath.  Two  years  ago  he  passed 
through  an  unusually  severe  typhoid  fever,  from  which  he  made 
a  good  recovery  with  the  single  exception  of  sudden  attacks  of 

rapid,  violent  beating  of  the  heart,  that  almost  invariably  came  on 
46 


706  DISEASES  OF  THE  HEART 

shortly  after  a  meal.  They  were  accompanied  and  followed  by  a 
feeling  of  exliaustion,  and  were,  naturally  enough,  very  alarming 
to  both  the  patient  and  his  family.  The  attacks  were  of  frequent 
occurrence,  sometimes  daily,  I  examined  the  young  man  at  that 
time  and  was  unable  to  discover  any  indication  whatever  of  car- 
diac disease. 

The  history  of  a  recent  severe  typhoid  fever  made  me  con- 
sider the  possibility  either  of  an  acute  myocarditis  during  his  ill- 
ness or  of  the  myocardium  having  been  seriously  enfeebled  in  con- 
sequence of  fatty  degeneration,  such  as  has  been  so  well  described 
by  Quain.  But  the  heart's  dulneso  and  the  heart-sounds  were  nor- 
mal, and  inquiry  elicited  the  statement  that  he  was  able  to  exer- 
cise, indeed  had  but  just  returned  from  a  shooting  trip  in  the 
mountains  of  North  Carolina,  without  experiencing  any  shortness 
of  breath,  vertigo,  or  palpitation.  The  pulse  was  rapid  during 
my  examination,  but  its  volume  and  force  were  excellent.  I  there- 
fore assured  him  that  his  attacks  were  of  a  functional  nature  and 
did  not  indicate  heart-disease. 

His  flesh  at  that  time  was  rather  too  flabby,  and  he  said  he 
had  been  gaining  weight  rapidly  since  his  recovery  from  his  fever. 
IMinute  inquiry  into  his  habits,  diet,  etc.,  brought  out  the  fact  that 
he  was  eating  enormously  and  altogether  too  much  carbohydrates, 
and  was  in  the  habit  of  drinking  a  large  amount  of  water  with 
his  meals.  He  acknowledged  some  feeling  of  being  bloated  after 
eating.  It  was  concluded,  in  the  absence  of  other  etiological  fac- 
tors, that  gastronomic  errors  were  at  the  bottom  of  his  complaint, 
and  he  was  advised  to  cut  out  his  sweets  and  starches,  to  limit  his 
consumption  of  fluids  at  meals,  to  drink  lithia  water  between 
meals,  and  to  begin  his  former  systematic  exercise  both  in  the 
gymnasium  and  out  of  doors. 

This  regime  was  faithfully  carried  out,  with  the  result  that 
his  palpitations  almost  entirely  disappeared.  During  the  follow- 
ing two  years  he  came  to  see  me  twice,  once  a  few  weeks  after  his 
initial  visit,  merely  to  report  progress,  and  the  second  time  to  re- 
ceive an  examination  for  life  insurance,  which  on  my  recommen- 
dation was  granted  him. 

This  past  week,  however,  he  came  again  with  liis  father,  who 
said  he  wanted  to  know  how  it  could  be  that  so  robust  a  young 
man  could  still  have  his  attacks  of  palpitation  without  there  being 


FUNCTIpNAL   DISORDERS  707 

something  wrong  with  his  heart.  He  then  explained  that  the  Sun- 
day previous  his  son  was  about  to  start  for  church  with  his 
mother,  when  all  at  once  he  was  discovered  by  his  father  lying  on 
the  floor  and  his  heart  beating  so  fast  and  hard  that  it  could  be 
seen  through  the  clothes.     The  attack  lasted  about  twenty  minutes. 

The  young  man  then  spoke  up  and  said  he  did  not  see  any  use 
of  being  concerned  about  the  affair,  as  he  knew  perfectly  well  what 
had  brought  the  attack  on.  He  had  eaten  too  hearty  a  breakfast, 
consisting  of  coffee  and  three  pieces  of  German  coffee  cake,  besides 
fried  chicken  and  fruit.  An  examination  was  then  made,  and  a 
more  normal  heart  I  have  never  listened  to.  The  pulse  was 
steady,  regular,  and  80,  standing.  The  apex-beat  was  in  the  nor- 
mal situation,  absolute  dulness  was  not  increased,  and  the  rela- 
tive measured  3  inches  to  the  left  and  1  inch  to  the  right  of  the 
sternum.  The  sounds  were  clear,  of  normal  relative  intensity, 
and  entirely  free  from  murmurs  of  any  kind. 

It  was  without  hesitation,  therefore,  that  the  opinion  expressed 
two  years  previously  was  reiterated.  It  was  not  quite  clear  why 
the  attacks  should  take  place  in  so  powerful  and  an  apparently 
perfectly  well  young  man,  but  there  was  certainly  an  etiological 
connection  between  the  attacks  and  indiscretions  in  the  way  of  a 
too  liberal  allowance  of  carbohydrates.  There  was  either  a  tem- 
porary abeyance  of  vagus  control  or  a  stimulation  of  the  acceler- 
ator nerves  of  the  heart.  Whether  this  was  an  instance  of  reflex 
irritation  or  of  some  toxic  influence  resulting  from  indigestion, 
was  not  at  all  clear.  But  it  would  be  ordinarily  classified  as  a 
reflex  cardiac  neorosis. 

In  the  foregoing  case  precordial  pain  or  other  sensations  of 
an  allied  nature  were  never  complained  of.  It  is  quite  common 
for  an  attack  of  palpitation  to  be  accompanied  by  a  painful  sen- 
sation in  the  region  of  the  heart  or  for  the  exaggerated  cardiac 
action  to  follow  the  pain.  At  other  times  the  patient  may  com- 
plain of  the  heart's  pulsations  as  painful.  In  still  other  cases  the 
chief  complaint  is  of  an  indescribable  feeling  of  distress  or  dis- 
comfort "  at  the  heart,"  which  is  usually  but  not  invariably  at- 
tended or  succeeded  by  palpitation.  Such  symptoms  are  frequent 
in  individuals  who  are  hysterical.  This  class  of  cases  is  well 
illustrated  by  the  following  example : 

A  physician,  aged  twenty-four,  height  6  feet  1  inch,  weight 


708  DISEASES  OF   THE   HEART 

150  ijoiinds,  gave  a  history  of  "  heart-weakness  "  for  a  year.  His 
parents,  brothers,  and  sisters  were  all  living  and  in  good  health 
and  free  from  neurotic  tendency,  so  far  as  the  patient  knew. 
With  exception  of  measles  in  childhood  he  had  never  been  ill, 
and  he  denied  venereal  disease  or  sexual  excess,  and  did  not  use 
tobacco,  alcohol,  or  narcotics. 

During  the  siunmer  of  1899  he  had  been  particularly  hard 
worked  in  his  profession,  and  compelled  to  lose  much  sleep.  In 
iN^ovember  he  suddenly  developed  attacks  of  pain  in  the  region  of 
the  heart  that  were  speedily  followed  by  accelerated  forcible  beat- 
ing of  the  organ.  It  seemed  to  him  that  every  throb  of  the  heart 
produced  pain  just  below  the  left  nipple.  These  attacks  were  pre- 
cipitated by  exertion,  such  as  walking,  or  even  a  long  drive  into 
the  country.  After  they  had  endured  for  about  ten  days  he  be- 
came so  bad  that  he  used  to  faint  away  during  his  attacks,  and  he 
remained  unconscious  for  an  hour  or  more  in  spite  of  efforts  to 
revive  him. 

This  statement  made  me  suspicious  that  the  so-called  syncope 
was  not  in  reality  a  true  fainting  fit,  and  he  was  asked  if  he  be- 
came absolutely  insensible  to  his  surroundings,  or  whether  or  not 
he  knew  in  a  dim  w^ay  what  was  being  done  to  him.  He  then 
replied  that  he  believed  he  was  vaguely  conscious  of  his  surround- 
ings at  those  times. 

These  attacks  recurred  for  about  four  months,  and  were  finally 
cured  by  the  taking  of  |  of  a  grain  of  codeine  4  times  daily  dur- 
ing three  weeks.  The  drug  then  had  to  be  discontinued  because 
of  the  obstinate  constipation  it  occasioned.  During  those  four 
months  he  was  much  troubled  by  insomnia.  Since  April,  1900, 
his  condition  had  improved  somewhat,  but  at  the  date  of  his  ex- 
amination by  me,  October,  1900,  he  was  still  unable  to  endure 
exertion  because  of  the  palpitation  it  evoked. 

The  young  man  was  a  blond,  evidently  highly  nervous  and 
not  strong,  since  he  lolled  on  the  lounge  in  my  office,  as  though  too 
weak  to  sit  up.  His  hands  were  cold  and  moist,  and  his  arm  trem- 
bled while  the  pulse  was  being  examined.  This  was  full,  tense, 
regular,  and  varied  from  10.5  to  110.  The  apex-beat  was  in  the 
fifth  left  interspace  well  inside  the  nipple,  and  the  strong,  rather 
broad  shock  was  accompanied  In-  a  coarse  thiill.  Absolute  and 
relative   cardiac   dulness  were   normal,    the   latter   measuring   3 


FUNCTIONAL   DISORDERS  709 

inches  to  the  left  of  the  sternal  margin  and  1  inch  outside  the 
right  sternal  border. 

The  first  sound  at  the  apex  was  partially  obscured  by  a  rough 
vibrant  murmur  of  whizzing  quality,  which  was  loudest  in  the 
erect  position,  disappeared  in  the  fight  lateral  decubitus,  and  was 
scarcely  audible  when  the  patient  lay  on  his  left  side.  It  was 
increased  in  intensity  at  the  end  of  deep  inspiration  and  grew 
almost  inaudible  at  the  close  of  expiration.  The  second  pulmonic 
sound  was  not  accentuated. 

The  liver  was  not  palpable  and  its  dulness  did  not  pass  below 
the  inferior  costal  margin,  right  nipple-line.  The  abdomen  was 
negative.  The  patient  reported  his  urine  as  negative,  containing 
neither  albumin  nor  sugar.  He  was  not  conscious  of  indigestion, 
and  the  bowels  were  not  constipated. 

The  diagnosis  was  made  of  a  cardiac  neurosis  with  an  acci- 
dental murmur  and  palpitation. 

The  patient  was  advised  to  spend  the  winter  in  the  South, 
where  he  could  be  in  the  open  air,  to  take  moderate,  regular  exer- 
cise, and  endeavour  to  build  up  his  nervous  system,  and  to  school 
himself  to  regard  his  malady  as  not  organic.  In  the  way  of 
medication  he  was  advised  to  take  strychnine,  give  up  the  use  of 
digitalis  and  allied  heart  tonics.  Up  to  the  present  writing  I  have 
had  no  further  report  from  this  case. 

This  patient  illustrated  another  feature  of  hysterical  patients 
with  disordered  heart  action.  He  declared  he  was  always  con- 
scious of  its  pulsations,  and  could  tell  how  it  was  beating  without 
having  to  feel  his  pulse.  To  test  him  in  this  matter  I  took  hold 
of  the  wrist  and  counted  the  pulse,  and  then  told  him  to  count 
aloud  his  heart-beats.  In  this  he  utterly  failed,  and  I  became  con- 
vinced that  his  sensations  were  imaginary.  This  is  not  always 
the  case,  however,  for  in  some  instances  the  cardiac  action  is  suffi- 
ciently exaggerated  to  be  perceived  by  the  patient.  Sometimes, 
too,  when  the  pulse-tension  is  high  the  individual  can  perceive 
pulsations  in  the  extremities. 

The  powerful  influence  of  the  imagination  and  the  readiness 
with  which  an  attack  of  palpitation  can  be  elicited  by  trivial 
causes  are  illustrated  by  the  following  case : 

A  law  student,  aged  twenty-four,  sought  advice  because  of 
palpitations  since  the  age  of  fourteen.     Family  history  was  nega- 


710  DISEASES  OF  THE  HEART 

tive,  and  the  patient  had  not  suffered  from  any  acute  disease  that 
might  have  led  to  endocarditis  or  pericarditis.  lie  thought  his 
trouble  with  his  heart  dated  from  his  study  of  physiology  in 
school,  when  he  observed  that  his  pulse  was  too  rapid. 

At  all  events,  from  that  time  on  he  has  been  subject  to  fre- 
quent attacks  of  violent,  rapid  beating  of  the  heart,  and  has  been 
told  repeatedly  that  he  had  heart-disease.  He  is  greatly  fright- 
ened by  his  attacks,  which  often  come  on  without  apparent  cause 
or  when  fatigued  by  study,  during  unwonted  exercise  and  excite- 
ment, or  even  too  close  application  to  his  books.  He  is  greatly 
troubled  with  flatulence,  and  this  often  sets  the  heart  to  palpi- 
tating. During  an  attack  he  is  exhausted,  alarnied,  and  notices 
particularly  a  violent  beating  in  the  stomach.  Pollutions  occur 
every  two  or  three  weeks,  and  are  folloM'ed  next  day  by  extreme 
weariness,  nervousness,  and  liability  to  his  palpitations. 

Examination  showed  him  to  be  a  tall,  slender  man  with  thin 
chest  and  broad  intercostal  spaces.  The  abdomen  was  thin,  rather 
scaphoid  when  in  the  dorsal  decubitus,  and  the  abdominal  aorta 
pulsated  visibly.  There  was  gurgling  in  the  course  of  the  trans- 
verse colon,  but  no  dilatation  of  the  stomach,  and  no  demonstrable 
enteroptosis.  The  pulse  was  full,  soft,  rapid,  and  regular.  The 
action  of  the  heart  was  excited  and  abnormally  forcible,  and  the 
cervical  arteries  pulsated  strongly. 

The  apex-beat  was  in  the  normal  position,  cardiac  dulness  was 
not  increased,  and  the  sounds  were  clear,  but  too  ringing.  No 
murmurs  could  be  detected.  During  the  examination  the  patient 
became  very  nervous  and  exhibited  a  fine  tremor,  the  hands  being 
warm  and  moist. 

There  could  be  no  doubt  of  the  nature  of  his  fancied  heart- 
disease,  and  he  was  emphatically  assured  that  his  trouble  was  a 
neurosis  and  that  he  need  apprehend  no  danger  from  his  attacks. 
It  was  concluded  also  that  in  this  case  there  was  a  reflex  element, 
and  that  the  cause  of  his  palpitations  lay  in  such  an  excitability 
of  tlie  cardiac  accelerator  nerves  that  they  were  sensitive  to  con- 
ditions which  would  be  wholly  inadequate  to  arouse  them  in  a 
normal  individ'iuil.  Tlie  chronicity  of  the  affection  made  prog- 
nosis rather  unfavourable. 

So  much  suffering  was  caused  by  the  pollutions  that  the  ure- 
thra was  explored,  resulting  in  the  detection  of  nothing  more  than 


FUNCTIONAL  DISORDERS  Til 

hypera3sthesia  of  its  posterior  portion.  Local  treatment  was  in- 
stituted by  the  specialist  to  whom  the  patient  was  referred,  but 
with  no  appreciable  effect  on  his  attacks  of  palpitation. 

The  following  extremely  instructive  case  exemplifies  the  as- 
sociation of  a  veritable  phobia  with  a  distinct  hysterical  element 
and  a  reflex  irritation,  or  at  all  events  an  imaginary  reflex  irrita- 
tion: 

The  patient  was  a  German-American,  married,  aged  twenty- 
six,  of  medium  height  and  weight.  She  sought  medical  aid  be- 
cause of  "  weakness,  palpitation,  and  sinking  spells."  Her  fam- 
ily history  was  negative,  excepting  that  her  mother  and  sisters 
were  nervous.  The  patient  was  doubtful  concerning  her  having 
had  the  ordinary  diseases  of  childhood,  but  denied  rheumatism  or 
other  illness  of  an  acute  or  infectious  nature.  Said  she  had  had 
stomach  trouble  and  been  nervous  all  her  life,  and  at  ten  years  of 
age  had  heart-trouble  that  came  from  her  stomach  and  persisted 
about  a  year.  From  that  attack  she  recovered  without  treatment, 
and  she  remained  well  with  exception  of  nervousness  until  two  or 
three  years  before  marriage,  at  which  time  she  had  some  nervous 
trouble  that  lasted  a  year  and  a  half. 

During  her  pregnancy  she  suffered  much  with  her  heart  and 
stomach.  The  confinement  was  difficult,  necessitating  the  admin- 
istration of  chloroform  and  delivery  with  forceps.  She  thought 
the  chloroform  weakened  her  heart  very  much,  and  she  was  not 
strong  enough  to  nurse  her  baby.  That  was  two  and  a  half  years 
ago,  and  ever  since  she  has  been  a  nervous  wreck. 

She  has  "  heart  attacks  "  from  exercise,  excitement,  and  after 
eating.  These  have  been  much  worse  the  last  four  months  in 
spite  of  treatment,  and  last  week  came  as  often  as  twice  a  day. 
Excitement,  as  from  anger  or  domestic  wrangles,  which  unfortu- 
nately are  too  frequent,  at  once  give  her  a  sinking  spell,  and  she 
lies  exhausted  for  hours,  her  heart  beating  very  rapidly  at  such 
times,  occasionally  as  much  as  160  a  minute,  in  this  respect  re- 
sembling paroxysmal  tachycardia.  At  times  the  taking  of  some 
article  of  food  or  a  remedy  which  disagrees  with  her  stomach  will 
instantly  produce  palpitation  with  extreme  exhaustion.  At  these 
times  she  is  alarmed,  but  is  speedily  quieted  and  her  pulse  slows 
down  upon  the  arrival  of  a  physician.  She  thinks  she  has  been 
relieved  a  little  by  strophanthus,  and  has  very  strong  notions  re- 


712  DISEASES  OF  THE  HEART 

garding  the  effect  on  her  of  certain  medicaments — e.  g.,  dilute 
hydrochloric  acid,  which  twice  gave  her  a  violent  and  prolonged 
attack  of  palpitation. 

Her  symptoms  are  always  more  likely  to  occur  about  ten  days 
before  menstruation,  but  when  the  menses  have  become  estab- 
lished, her  heart  is  more  quiet  and  she  feels  better.  Attacks  are 
also  very  apt  to  follow  looseness  of  the  bowels,  and  conversely  are 
not  so  easily  called  forth  when  she  is  constipated.  Ever  since 
the  birth  of  her  child  she  has  been  subject  to  the  appearance  on 
her  extremities  of  "  spots  that  look  just  like  bruises,  are  dark  red, 
gradually  grow  yellowish  and  fade  away."  Of  late  she  has  eaten 
only  beef  and  wine,  because  anything  else  produced  gas  on  the 
stomach  and  the  attacks  of  palpitation  and  sinking  spells. 

She  notices  some  shortness  of  breath  on  fast  walking  and  as- 
cending stairs;  has  appetite,  and  could  eat  if  her  stomach  would 
let  her,  and  after  eating  her  stomach  feels  heavy.  The  bowel 
movements  are  irregular,  but  menses  are  regular,  lasting  two  days. 
Her  sleep  is  disturbed  by  palpitation,  and  she  nearly  always  feels 
dizzy.  During  the  rapid  heart's  action  she  notices  pulsation  in 
the  carotids  and  in  the  stomach,  and  she  has  a  feeling  as  if  her 
lungs  filled  up  with  blood,  her  face,  feet,  and  hands  are  cold,  and 
she  feels  also  as  if  she  could  not  breathe. 

The  attacks  persist  from  half  an  hour  to  several  hours,  and  are 
not  followed  by  a  flow  of  copious  pale  urine.  In  a  word,  there  is, 
excepting  severe  pain,  scarcely  a  sensation  connected  with  the 
heart  of  which  this  highly  neurotic  and  imaginative  woman  does 
not  complain.  It  is  apparent  that  she  is  only  too  glad  and  ready 
to  talk  and  dilate  upon  her  symptoms.  She  is  sure  she  is  going 
to  die  in  one  of  her  attacks. 

Physical  examination  showed  pulse  106,  small,  regular,  but 
not  of  noticeably  low  tension,  and  carotids  throbbed  slightly. 
Apex-beat  was  in  fifth  left  interspace,  3^  inches  from  midsternal 
line,  and  accompanied  by  a  slight  thrill,  which  disappeared  in  the 
recumbent  posture,  although  the  apex-shock  became  more  defined. 
Relative  cardiac  dulness  reached  from  1  inch  to  right  of  sternum 
to  3|  inches  to  the  left  of  that  l)one.  The  first  sound  was  accom- 
pained  by  a  faint,  short,  high-pitched  systolic  whiff,  which  was  of 
limited  transmission  upward  and  to  right  and  was  slightly  louder 
at   end    of    inspiration — and    both    jiuliiionic    and    aortic    second 


FUNCTIONAL  DISORDERS  Y13 

sounds  seemed  accentuated.  In  the  standing  position  the  abdomen 
bulged  relatively  too  much  below  and  was  too  flat  above  the  um- 
bilicus. The  right  kidney  descended  to  a  little  below  the  costal 
arch,  but  could  not  be  grasj)ed.  The  liver  could  not  be  made  out 
as  having  dropped  downward.  Gastric  tympany  reached  3  inches 
below  and  1  inch  too  far  to  right  of  the  umbilicus,  and  there  was 
splashing.  The  abdominal  aorta  pulsated  with  abnormal  force, 
but  could  not  be  distinctly  palpated.  The  abdominal  viscera 
evidently  dragged  somewhat  upon  their  supports,  and  gas- 
troptosis  was  undoubtedly  present.  The  pelvic  organs  were  nega- 
tive. The  lungs  were  negative,  and  there  was  no  oedema  about 
the  ankles. 

A  week  subsequently,  after  having  been  limited  to  two  meals 
a  day,  and  having  enjoyed  a  week  of  immunity  from  her  attacks, 
her  heart's  action  was  found  slow  but  somewhat  irregular  in  fre- 
quency. The  apex-thrill  previously  noted  was  discovered  to  be  a 
short  but  very  distinct  presystolic  one,  and  the  first  sound  was 
unmistakably  thumping.  Upon  the  patient  assuming  the  recum- 
bent posture  the  second  sound,  exactly  at  the  seat  of  apex,  was 
doubled  and  a  low-pitched  short  murmur  accompanied  the  first 
sound.  I  was  therefore  forced  to  conclude  that  this  patient  had 
mitral  stenosis,  l^evertheless,  her  symptoms  were  those  of  a  car- 
diac neurosis  rather  than  of  an  organic  lesion. 

She  was  sent  to  a  well-known  neurologist,  who  reported  that, 
although  distinct  hysterical  stigmata  were  not  discoverable,  he 
yet  believed  there  was  an  hysterical  element  in  the  case.  In  addi- 
tion, I  could  not  rid  myself  of  the  belief  that  the  condition  of  the 
stomach  and  bowels  had  much  to  do  with  the  production  of  her 
attacks.  At  one  time  they  w^ould  follow  an  indigestible  meal  or 
a  relaxation  of  the  bowels  sufficient  to  merit  the  term  of  diarrhoea, 
at  another  some  emotional  disturbance,  as  a  quarrel  with  her  hus- 
band or  an  ungratified  sexual  desire — in  short,  a  considerable 
variety  of  disturbing  causes. 

This  case  gave  me  endless  trouble  and  perplexity,  until  at 
last,  acting  on  a  hint  furnished  by  her  statements  concerning  the 
etiological  influence  of  diarrhoea,  I  prescribed  a  combination  of 
astringents  which  kept  her  bowel  somewhat  constipated.  She  then 
became  more  and  more  free  from  her  fearful  attacks,  and  with  in- 
creasing freedom  from  them  regained  a  measure  of  confidence,  so 


714  DISEASES  OF  THE  HEART 

that  at  the  present  writing,  1901,  I  have  not  seen  her  for  nearly 
two  months. 

Augtist,  1902,  heart's  action  heing  quiet,  there  was  entire  absence  of  cardiac 
murmurs,  and  the  organ  was  to  all  apjpearances  free  from  disease.  The  presystolic 
murmur  and  doubling  of  second  sound  above  noted  must  therefore  have  been  of  acci- 
dental origin  a/nd  in  some  way  due  to  the  disturbed  cardiac  rhythm. 

A  clergyman's  widow,  German,  consulted  me  because  she  was 
sure  s(miething  was  wrong  with  her  heart,  and  she  feared  she  was 
suffering  from  the  disease  her  husband  died  of.  This  was  Grave.s's 
disease,  the  man  having  been  frequently  seen  by  me  during  his 
life  and  final  illness.  For  two  years  after  his  death  she  remained 
in  her  usual  health,  but  about  a  year  ago  she  began  to  suffer  from 
"  si)ells  with  her  heart,"  which  were  brought  on  by  excitement, 
and  sometimes,  she  thought,  by  the  taking  of  food  that  did  not 
agree  with  her  stomach,  for  with  the  eructation  of  gas  the  palpi- 
tation began.  At  still  other  times  the  attacks  came  on  without 
any  apparent  cause. 

The  action  of  the  heart  was  likened  to  "  rope  jumping."  She 
feels  a  "  clutch  at  the  heart,"  then  her  heart  begins,  and  the  next 
moment  she  is  "  entirely  gone,"  the  face  being  "  deathly  pale  and 
the  hands  cold  as  ice."  Nothing  relieves  her  so  quickly  as  a  little 
brandy.  Last  week  she  had  two  attacks.  She  said  she  often 
noticed  a  gurgling  in  the  left  side  of  her  abdomen,  and  this  gave 
her  much  uneasiness.  Her  appetite  was  poor,  and  she  was  in  the 
habit  of  drinking  coffee  four  or  five  times  a  day.  She  was  con- 
stipated, but  her  menses  were  regular.  Her  account  of  her  com- 
plaint was  not  that  of  a  neurasthenic,  and  there  was  nothing  in 
her  symptoms  or  appearance  to  suggest  that  she  belonged  to  that 
class  of  sufferers.  Neither  was  there  any  history  of  neurotic  dis- 
turbances in  her  family. 

She  was  thirty  years  of  age,  rather  spare,  and  of  medium 
height.  There  was  no  throbbing  of  the  carotids,  no  tremor,  no 
perspirations,  no  enlargement  of  the  thyroid — in  short,  no  indica- 
tion of  Graves's  disease.  Tlie  ])ulse  was  90,  equal,  regular,  and  of 
fair  tension.  The  apex-beat  was  in  the  normal  situation,  cardiac 
dulness  was  normal,  and  the  heart-sounds  were  normal  excepting, 
perhaps,  that  the  first  was  rather  too  ringing.  There  were  no 
murmurs.  The  lungs  were  negative  also.  Within  the  abdomen 
was  the  interesting  finding  that  acconnled  for  licr  gurgling.     The 


FUNCTIONAL  DISORDERS  Tl5 

abdominal  walls  were  relaxed,  depending  baglike  and  bulging  in 
the  hypogastrinm,  while  the  epigastric  region  was  too  flat.  An 
indistinct  splashing  was  elicited,  and  gastric  tympany  extended 
well  down  into  the  pelvis,  but  not  more  than  an  inch  to  the  right 
of  the  median  line.  It  began  at  the  level  of  the  ninth  instead  of 
the  seventh  costal  cartilage,  and  was  too  long  vertically  in  propor- 
tion to  its  lateral  dimensions.  The  kidneys  and  other  viscera 
could  not  be  made  ont  as  prolapsed.     She  looked  ansemic. 

Here,  then,  was  an  individual  whose  organs  were  apparently 
normal  with  exception  of  the  stomach,  which  was  prolapsed  but 
not  dilated.  !No  other  condition  could  be  discovered  to  account 
for  her  palpitations,  and  accordingly  she  was  told  that  the  attacks 
were  probably  due  to  the  gastric  disorder,  perhaps  intensified  by 
the  undue  use  of  cofi:"ee.  She  was  emphatically  assured  that  her 
attacks  were  not  dangerous  and  was  ordered  to  secure  an  abdom- 
inal supporter,  and  so  adjust  her  clothing  as  to  avoid  the  dragging 
of  her  skirts  upon  the  abdominal  parietes  and  pressure  upon  her 
stomach. 

She  was  given  tincture  of  nux  vomica  before  and  dilute  hydro- 
chloric acid  in  essence  of  pepsin  after  meals.  For  the  attack  of 
palpitation  with  pallor  of  face  and  coldness  of  the  extremities  she 
was  given  tablets  of  nitroglycerin.  Coifee  was  forbidden,  and  in- 
structions were  given  regarding  a  simple  and  nourishing  diet.  At 
present  Avriting  the  symptoms  still  persist,  but  are  less  severe. 

Tachycardia. — The  physician  is  frequently  called  on  to  treat 
cases  of  habitually  rapid  heart's  action,  which  are  so  annoying  to 
the  patient  by  reason  of  his  subjective  consciousness  of  the  same 
that  they  may  be  said  to  be  a  persistent  palpitation.  In  many  in- 
stances this  is  the  exaggerated  cardiac  action  of  Graves's  disease, 
yet  it  is  so  prominent  a  symptom  that  it  brings  the  patient  to  the 
doctor  in  the  belief  that  the  heart  is  the  real  seat  of  the  trouble. 
As  exophthalmic  goitre  is  a  disorder  of  the  nervous  system  instead 
of  the  heart,  it  will  not  receive  special  consideration  in  this  work. 
There  is  another  class  of  cases,  however,  which  likewise  present 
tachycardia  and  attacks  of  palpitation  as  their  main  symptoms, 
and  which  because  sometimes  associated  with  thyroid  enlargement 
would  seem  to  be  incomplete  forms  of  Graves's  disease.  The  indi- 
viduals are  highly  nervous,  easily  agitated,  manifest  more  or  less 
tremor,  and  in  some  instances  have  a  warm  unduly  perspiring 


716  DISEASES  OP  THE  HEART 

skin.  They  do  not  show  cxoplithahiios,  and  if  goitre  is  not  pres- 
ent, it  is  often  exceedingly  difficult  to  say  whether  they  belong  to 
the  category  of  exophthalmic  goitre  or  not.  Most,  if  not  all,  the 
cases  I  have  seen  have  been  in  women,  who,  as  a  rule,  are  below 
the  age  of  forty. 

T  have  frequently  discovered  enteroptosis  in  these  persons,  and 
I  am  not  able  to  escape  the  conviction  that  there  is  some  intimate 
etiological  connection  between  this  condition  and  that  of  the  nerv- 
ous system.  In  some  there  has  been  evidence  of  moderate  cardiac 
hypertrophy  and  in  others,  not. 

This  form  of  cardiac  neurosis,  as  it  may  not  inaptly  be  termed, 
was  well  illustrated  by  the  case  of  a  married  woman  of  twenty- 
seven  who  came  for  treatment  on  account  of  symptoms  that  made 
her  fear  heart-disease.  One  sister  had  died  of  pulmonary  tuber- 
culosis at  the  age  of  twenty-four,  and  I  may  say,  in  passing,  that 
in  my  cases  I  have  been  struck  by  the  frequency  with  which  a 
history  of  consumption  in  some  near  relative  has  been  obtained. 
The  patient  had  not  been  in  her  previously  good  health  since  her 
last  confinement,  two  and  a  half  years  before.  Her  home  was  in  a 
remote  suburb  in  a  lonely  situation,  and  as  night  approached  and 
her  husband  did  not  return  she  regularly  grew  nervous  and  appre- 
hensive. She  had  lost  weight,  and  for  a  considerable  time  had 
noticed  that  her  heart  beat  too  fast.  Recently  it  had  taken  to 
giving  a  "  flop,"  and  every  time  this  occurred  it  threw  her  into 
a  state  of  alarm  and  agitation.  Her  neck  had  grown  full,  but  she 
had  given  this  no  attention  in  comparison  with  the  action  of  her 
heart.  She  was  a  hearty  feeder,  and  all  her  functions  appeared  to 
be  normal.  Physical  examination  showed  pronounced  enlarge- 
ment of  the  thyroid,  which  was  firm  and  without  thrill.  There 
was  no  prominence  of  the  eyeballs,  but  there  w^as  a  fine  tremor 
and  the  pulse  was  so  rapid,  in  consequence  of  extreme  nervous  agi- 
tation, that  no  attempt  was  made  to  count  it.  Cardiac  impulse 
was  exaggerated,  but  the  area  of  dulness  was  not  demonstrably 
increased,  and  the  sounds  were  clear,  ringing,  and  free  from  mur- 
murs. The  lungs  were  negative  and  there  was  no  enteroptosis. 
The  case  was  regarded  as  one  of  incomplete  exophthalmic  goitre, 
and  a  guarded  prognosis  was  expressed.  The  patient  was  assured 
that  she  had  no  heart-disease,  and  T  observed  that  this  assurance 
at  once  favourably  influenced  the  heart's  action  and  nervousness. 


FUNCTIONAL  DISORDERS  717 

In  conclusion,  it  may  be  stated  that  under  the  prolonged  use 
of  iodine  to  the  neck  and  internal  medication  addressed  to  relief 
of  symptoms  and  improvement  of  digestion  and  general  health, 
this  patient  ultimately  made  a  complete  recovery,  the  thyroid 
becoming  of  normal  size  and  the  tachycardia  disappearing  en- 
tirely. There  was  evidently  a  neurosis  in  this  case,  as  shown  by 
the  powerful  domination  of  her  emotions  over  the  action  of  her 
heart.  Whether  there  was  any  direct  connection  between  the  thy- 
roid enlargement  and  the  tachycardia  and  palpitations  I  am  not 
able  to  say,  but  her  nervousness  certainly  disappeared  pari  passu 
with  the  decrease  in  the  size  of  the  gland.  ISTevertheless,  her 
pulse-rate  was  invariably  influenced  by  the  state  of  her  digestion 
and  elimination. 

I  recall  another  case  of  rapid  and  pounding  cardiac  action 
in  a  female  who  presented  fine  tremor  of  the  extremities,  but  no 
other  signs  of  Graves's  disease,  and  who  was  ultimately  found  to 
be  pregnant  at  the  time.  As  she  was  positive  that  her  symptoms 
had  first  attracted  her  notice  after  the  cessation  of  her  menses, 
and  the  heart's  action  quieted  down  somewhat  as  the  pregnancy 
advanced,  I  have  not  been  able  to  determine  what  the  connec- 
tion, if  any,  was  between  the  two  conditions.  This  patient  was 
unmistakably  neurotic,  as  shown  by  both  her  family  and  personal 
history.  Whether  such  cases  are  instances  of  incipient  or  incom- 
plete Graves's  disease  or  not,  they  are  instances  of  cardiac  neuro- 
sis so  far  as  the  action  of  the  heart  is  concerned. 

The  foregoing  cases  present  some  of  the  symptomatology  of 
heart-neuroses  so  graphically  that  it  was  thought  best  to  intro- 
duce them  before  considering  the  etiology,  although  in  so  doing 
the  general  plan  of  this  work  is  departed  from.  It  is  believed 
they  will  throw  some  light  on  the  causation  of  some  of  the  most 
common  manifestations  of  functional  cardiac  disorders.  As  there 
is  no  demonstrable  alteration  in  the  structure  of  the  refractory 
organ  in  typical  cases,  there  is  no  morbid  anatomy  to  be  described. 
If  a  valvular  lesion  or  dilatation  of  the  heart  is  found  in  a  person 
displaying  the  symptoms  of  neurotic  disturbance  of  cardiac  ac- 
tion, a  combination  which  is  not  at  all  infrequent,  the  anatomico- 
pathological  changes  on  the  part  of  the  heart  are  not  to  be  re- 
garded as  dependent  upon  the  neurosis.  There  may  be  an  etiologi- 
cal connection  in  so  far  as  the  organic  heart-lesion  may,  through 


718  DISEASES  OF  THE   HEART 

its  influence  over  metabolism,  aid  in  the  development  or  the  main- 
tenance of  the  neurosis  and  may  help  to  explain  the  ease  with 
which  the  heart's  action  is  perturbed.  It  may  also  be  claimed  that 
the  palpitation  and  tachycardia  induce  the  dilatation;  but  in  my 
experience  these  cases  do  not  display  permanent  cardiac  enlarge- 
ment to  an  extent  that  calls  for  treatment. 

As  previously  stated,  the  pathology  of  palpitation  is  ohsciire.  It 
is  argued  that  it  may  be  due  to  loss  of  vagus  control,  which  allows 
the  accelerator  to  gain  the  ascendency,  or  that  there  may  be  stimu- 
lation of  this  latter  independent  of  an  abeyance  of  the  inhibitory 
apparatus.  Again,  it  is  not  at  all  certain  that  there  may  not  exist 
some  histological  change  in  the  heart  structures  or  nerve-centres 
which  may  account  for  the  readiness  with  Avhich  the  action  of  the 
heart  becomes  disturbed  under  conditions  that  are  inoperable  in 
the  healthy  individual.  As  Romberg  saj^s,  arteriosclerosis  some- 
times develops  in  neurasthenics  at  an  unusually  early  period  of 
life;  and  who  can  say  that  there  may  not  be  some  connection  be- 
tween this  fact  and  the  cardiac  manifestations  ?  These  are  mat- 
ters of  speculation  purely,  and  in  the  present  state  of  our  knowl- 
edge we  must  content  ourselves  with  speculation  and  theory. 

Cardiac  Pain. — This  is  another  exceedingly  frequent  symptom 
in  neurotic  patients  who  suffer  from  fancied  disease  of  the  heart. 
It  possesses  no  uniformity  in  intensity  or  character,  being  in  one 
case  sharp  and  darting,  in  another  dull  and  continuous.  Its  one 
feature,  common  to  all,  is  its  location  in  the  heart-region,  usually 
in  close  proximity  to  the  left  nipple.  It  is  sometimes  intensified 
or  even  evoked  by  exercise — e.  g.,  sweeping,  which  calls  into  use 
the  muscles  of  that  portion  of  the  chest.  In  some  instances  it 
seems  to  be  influenced,  in  part  at  least,  by  atmosplieric  conditions. 
Very  frequently  this  pain  is  associated  with  a  feeling  of  anxiety 
or  oppression  in  the  prtecordia,  which,  because  it  occasions  a  vague 
feeling  of  apprehension,  is  by  the  Germans  called  herz  angst,  or 
anxiety  of  the  heart. 

This  sensation  may  be  wholly  independent  of  any  demon- 
strable change  in  the  heart  action,  but  is  apt  to  be  attended  by 
palpitation,  coldness  of  the  hands  and  feet,  and  other  indications 
of  vaso-motor  disturbance.  As  stated,  it  may  accompany,  but  as 
a  rule  it  seems  to  replace,  actual  pain.  Whatever  the  exact  char- 
acters of  this  j)ru'Cordial  feeling,  it  is  very  unlike,  and  is  not  to 


FUNCTIONAL  DISORDERS  719 

be  confounded  with  tlio  painful  seizures  wliicli  are  designated 
angina  pectoris,  whether  true  or  false.  The  differences  are  so 
marked  that  no  mistake  ought  to  be  made,  and  yet  it  is  possible 
for  the  feeling  of  cardiac  anxiety  to  be  mistaken  for  the  constric- 
tion of  the  chest  present  in  grave  angina  and  the  feeling  of  appre- 
hension for  the  sense  of  impending  death. 

Pseudo-angina  Pectoris. — From  the  standpoint  of  scientific  ac- 
curacy this  term  may  be  and  doubtless  is  objectionable,  since  there 
can  be  no  such  thing  as  a  false  chest  pain.  jSTevertheless,  this 
term  is  sanctioned  by  the  usage  of  the  best  writers  in  this  country 
and  Europe.  It  includes  those  precordial  pains  which  closely  re- 
semble attacks  of  coronar^^  angina,  and  are  therefore  spoken  of  by 
Osier  as  "  allied  states."  The  essential  difference  between  them 
lies  in  the  fact  that  pseudo-angina  is  independent  of  structural 
disease  of  the  heart  or  its  nutrient  vessels,  and  that  it  is  not  likely 
to  cause  sudden  death. 

In  true  angina  there  is  some  condition  within  the  heart  which 
initiates  the  stimulus  sent  to  the  nerve-centres.  In  the  pseudo 
form  the  starting-point  of  the  painful  attack  is,  according  to 
Huchard,  not  the  heart,  but  some  peripheral  or  visceral  nerve, 
most  commonly  one  of  the  intercostals.  The  impulse  thence  passes 
to  the  medulla,  and  there,  reaching  the  sensory  centres,  evokes  a 
sensation  of  pain  that  radiates  into  the  chest  or  down  the  arm 
with  phenomena  that  point  to  a  coincident  stimulation  of  the  vaso- 
motor and  vagus  centres.  Often  it  is  some  painful  point  on  the 
chest,  generally  one  in  the  region  of  the  left  nipple,  which  acts  as 
the  starting-place  for  an  attack.  Whether  such  is  the  pathology  of 
these  cases  or  not,  it  certainly  seems  to  me  to  afford  a  fairly  satis- 
factory explanation  of  the  essential  difference  betw^een  these  two 
forms  of  angina. 

Writers  recognise  three  great  varieties  of  this  neurotic  form: 
the  reflex,  the  vaso-motor,  and  the  toxic.  Of  these,  angina  re- 
flectoria  is  the  most  common,  although  no  one  can  observe  these 
cases  without  coming  to  the  conclusion  that  they  are  all  very  apt 
to  blend  indistinguishably  with  each  other.  Irritation  within  the 
abdominal  organs  is  thought  to  be  the  most  common  starting-point 
of  an  attack  of  the  reflex  variety,  and  yet  the  vaso-motor  form 
may  likewise  find  its  origin  in  some  disturbance  within  the  abdo- 
men as  well  as  in  any  part  of  the  body.     Huchard  dwells  much  on 


720  DISEASES  OF  THE  HEART 

the  toxic  angina  and  finds  its  cansation  in  toxic  agencies  intro- 
dnced  into  the  system  from  without,  snch  as  tobacco. 

An  attack  of  pseudo-angina  pectoris  is  agonizing,  and  because 
it  usually  begins  in  the  cardiac  area  it  excites  a  feeling  of  fear  or 
apprehension  that  is  closely  allied  to  a  sense  of  impending  death. 
Ordinarily,  however,  the  patient  admits  that  this  feeling  is  subor- 
dinate to  that  of  pain.  This  latter  radiates  throughout  the  chest 
and  into  the  left  arm,  which  is  apt  to  feel  numb  and  cold.  There 
is  often  a  "  clutching  feeling  at  the  heart,"  and  the  patient  is  apt 
to  have  a  sensation  as  if  she  were  "  sinking  away."  At  such  times 
the  pulse  is  said  to  become  "  very  low,"  by  which  seems  to  be 
meant  slow  and  weak.  In  cases  of  the  vaso-motor  type  the  face  is 
pale  and  anxious,  the  extremities  cold  and  clammy,  and  the  pulse 
is  small,  usually  slow,  and  often  irregular  or  intermittent. 

The  sufferer  from  pseudo-angina  is  not  compelled  to  assume 
an  erect,  motionless  attitude,  as  in  true  angina,  but  lying  on  the 
bed  or  couch  moves  about  restlessly  and  moans  or  cries  aloud  with 
pain.  It  is  this  feature  of  the  attack  on  which  reliance  is  chiefly 
placed  in  the  determination  of  its  real  nature.  Exceptionally, 
patients  pass  into  a  cataleptic  state,  apparently  though  not  actu- 
ally unconscious,  rigid,  and  it  may  be  cold,  presenting  in  this 
state  an  appearance  which  is  very  alarming  to  the  friends,  who 
think  it  presages  speedy  death.  The  attacks  usually  come  on  sud- 
denly and  without  warning,  frequently  at  night,  but  in  some  in- 
stances there  are  prodromata,  such  as  chilliness,  restlessness,  or 
vague  nervous  sensations.  Some  authors  state  that  this  neurotic 
form  of  angina  displays  a  tendency  to  periodicity  by  recurring  at 
the  same  hour  on  successive  days. 

The  duration  of  the  seizures  is  longer  than  that  of  true  angina, 
lasting  for  one  or  more  hours ;  their  departure  is  apt  to  leave 
the  patient  weak  and  exhausted.  They  may  abate  gradually  or 
suddenly  or  they  may  terminate  in  an  attack  of  violent  palpita- 
tion. Numbness  and  helplessness  of  the  arm  into  which  the  pain 
radiates  are  not  infrequent  sequels  of  a  paroxysm.  Patients  are 
naturally  terrified,  not  only  by  the  seizure,  but  also  by  the  pros- 
pect of  its  return.  Its  frequency  of  occurrence  is  variable,  but 
usually  the  intervals  of  freedom  from  pain  are  not  long.  Hu- 
chard  observed  cases  in  Avhicli  as  many  as  200  or  300  attacks  were 
experienced  In  tlie  course  of  a  single  year. 


FUNCTIONAL  DISORDERS  721 

In  pure  angina  reflectoria  without  vaso-motor  phenomena 
irritation  originates  in  some  distant  part  and  the  pain  radiates 
thence  into  the  cardiac  area^,  from  which  it  spreads  along  the  in- 
tercostal nerves  and  even  into  the  left  arm.  There  is  usually  an 
associated  feeling  of  anxiety  and  constriction,  but  the  neuralgic 
element  is  the  more  pronounced,  Iluchard  cites  a  case,  not  ob- 
served by  himself,  however,  in  which  the  paroxysms  of  pain  origi- 
nated in  the  cicatrix  of  a  wound  received  many  years  before. 
This  was  situated  at  the  bend  of  the  elbow,  and  the  attack  of  pain 
was  precipitated  by  movements  of  the  joint,  by  friction  of  the 
clothing,  and  even  by  gentle  stroking  of  the  scar.  Squeezing  of 
the  middle  finger  was  also  capable  of  arousing  a  paroxysm,  and 
this  fact  together  with  their  cure  by  acupuncture  led  him  to  con- 
clude there  must  have  been  an  hysterical  element  in  the  case. 
He  also  quotes  the  instance  of  an  officer  who  experienced  an 
attack  of  pseudo-angina  in  consequence  of  painful  irritation  of  his 
foot  by  one  of  his  decorations,  which  had  fallen  into  his  boot,  and 
there  remained  during  the  day.  In  such  an  individual  there  must 
be  a  highly  neurotic  tendency.  Osier  narrates  a  single  case  in 
which  this  form  of  angina  followed  attacks  of  vomiting,  and  there- 
fore appeared  due  to  gastro-intestinal  irritation.  Such  attacks 
have  also  been  known  to  result  from  exposure  to  cold. 

In  the  vaso-motor  foi^m  the  exciting  cause  may  likewise  be 
exposure  to  cold  or  even  the  washing  of  the  hands  in  very  cold 
water.  In  this  group  there  are  phenomena  of  widespread  vaso- 
motor spasm  as  well  as  pain,  as  might  be  expected. 
•  The  strictly  toxic  form  is  exceedingly  uncommon  and  presents 
considerable  diversity  as  regards  the  severity  of  the  attacks  and 
the  prominence  of  certain  features.  Pain  is  often  subordinate  to 
a  feeling  of  anxiety  or  prsecordial  oppression  and  there  is  dis- 
turbed cardiac  rhythm  in  the  way  of  retardation  or  acceleration, 
irregularity,  and  intermittence  of  the  pulse.  In  tobacco  angina 
there  may  be  vertigo,  pallor,  a  contracted  pulse,  tendency  to  syn- 
cope, prsecordial  anxiety,  coldness  of  the  hands  and  feet,  and  cold 
perspirations.  According  to  Iluchard,  there  may  be  other  asso- 
ciated symptoms  which  are  referable  to  nicotine  intoxication,  as 
dizziness,  tinnitus  aurium,  dysphagia,  and  cephalalgia,  a  sense  of 
suffocation  or  dyspnoea,  general  weakness,  cerebral  confusion, 
spinal  tenderness,  and  disorders  of  vision.  Although  anginal 
47 


722  DISEASES  OF  THE   PIEART 

attacks  from  tobacco  may  be  incomplete  in  all  their  manifesta- 
tions, they  are  none  the  less  severe,  and  may  be  of  great  intensity. 

Etiology. — Althongh  the  automatic  action  of  the  heart  prob- 
ably depends  upon  some  quality  inherent  in  the  cardiac  muscle- 
cells,  and  not  upon  the  nerve  filaments  or  ganglia  situated  in  the 
heart-walls,  still  there  can  be  no  doubt  of  the  powerful  influence 
of  mental  and  nervous  states  ui)on  cardiac  action.  The  class  of 
disorders  now  considered  is  generally  thought  independent  of 
structural  disease  of  the  heart,  although  persons  with  organic  car- 
diac lesions  may  undoubtedly  present  some  symptoms  closely  akin 
to  those  of  the  so-called  cardiac  neuroses. 

The  predisposing  causes  of  the  so-called  functional  or  neurotic 
disturbances  of  cardiac  action  and  of  the  various  sensations  refer- 
able to  the  heart  are  those  disorders,  neurasthenia,  hysteria,  etc., 
which  for  want  of  definite  knowledge  of  their  pathology  are  called 
neuroses.  Psychoses,  such  as  hypochondria,  may  also  be  attended 
by  disturbance  of  cardiac  action  and  other  symptoms  referable 
to  the  heart.  Consequently  in  every  case  of  cardiac  neurosis  the 
physician  should  endeavour  to  ascertain  and  expect  to  deal  with 
some  such  underlying  neurotic  or  psychical  element. 

Heredity,  age,  and  sex  have  an  undoubted  etiologic  influence 
over  functional  disorders  now  considered.  Most  of  these  patients 
present  a  clear  family  history  of  neuroses,  and  some  of  them  have 
manifested  unstable  cardiac  action  from  childhood.  It  is  particu- 
larly in  the  female  sex  that  the  symptoms  which  have  been  de- 
scribed are  encountered,  and  yet  some  of  the  most  pronounced 
cases  are  seen  in  young  men.  Women  appea  especially  prone  to 
these  symptoms  during  the  child-bearing  period  and  at  the  meno- 
pause. Their  attacks  of  palpitation,  heart-pain,  or  what  not,  are 
very  apt  to  be  evoked  during  the  days  immediately  preceding 
menstruation.  This  is  not  because  of  any  direct  etiologic  connec- 
tion between  the  two,  but  simply  because  at  this  time,  as  at  the 
climacteric,  the  nervous  system  is  more  than  usually  unstable. 
Whatever  serves  to  lower  nerve  tone,  or  otherwise  deteriorate  the 
general  health,  predisposes  to  cardiac  neuroses,  and  therefore  mas- 
turbation, excessive  venery,  loss  of  sleep,  sorrow,  worry,  too  close 
confinement  to  mental  pursuits,  are  all  predisposing  factors. 

The  influences  which  act  as  exciting  causes  are  too  numerous 
and  various  and  often  too  obscure  to  warrant  the  attempt  to  enu- 


FUNCTIONAL  DISORDERS  723 

mcrate  them  in  detail.  Patients  are  very  apt  to  speak  of  having  a 
"  nervous  shock,"  by  which  may  be  meant  some  sudden  start  or 
fright,  an  unexpected  piece  of  bad  news,  and  the  like.  In  many 
instances  the  mere  suggestion,  whether  subjective  or  made  by  an- 
other, that  they  have  heart-disease  suffices  to  excite  an  attack  of 
palpitation.  This  is  particularly  the  case  with  hysterical  sub- 
jects, and  I  have  known  a  word  casually  dropped,  by  being  wrong- 
ly understood  to  apply  to  himself,  to  throw  such  a  person  into  a 
violent  fit  of  palpitation  with  coldness  of  the  hands  and  a  feeling 
of  intense  anxiety.  On  the  other  hand,  a  reassuring  word  will 
sometimes  as  promptly  quiet  the  action  of  the  heart. 

There  is  often  a  close  connection  between  the  taking  of  food 
or  a  remedy  and  the  onset  of  symptoms.  This  is  sometunes 
doubtless  the  result  of  suggestion,  at  others  of  the  formation  of 
products  of  indigestion,  and  when  this  latter  is  the  case  it  is  dif- 
ficult to  say  whether  it  is  through  a  reflex  or  mechanical  action 
or  is  the  eifect  of  the  absorption  of  toxins.  The  symptoms  not 
infrequently  come  on  so  quickly  that  there  would  hardly  seem  to 
be  time  for  the  formation  and  action  of  toxins.  In  neurasthenic 
individuals  fatigue  is  undoubtedly  an  exciting  factor.  I  have 
known  a  woman  to  take  a  short  walk  and  immediately  upon  her 
return  to  be  seized  by  a  sinking  spell  with  either  rapid  or  slow 
and  feeble  pulse  and  coldness  of  the  extremities,  symptoms  easily 
thought  to  indicate  heart-failure,  yet  in  reality  due  not  at  all  to 
cardiac  weakness.  Ordinarily  in  cardiac  neuroses  an  attack  of 
palpitation  is  not  produced  by  a  reasonable  amount  of  exercise. 
In  fact,  moderate  exercise,  as  walking,  is  more  likely  to  quiet 
down  the  heart.  N^evertheless  exceptions  may  occur,  as  was  the 
case  with  one  of  my  patients,  a  highly  neurotic  young  man  with- 
out demonstrable  signs  of  organic  disease. 

Cases  of  pseudo-angina  reflisctoria  have  been  shown  in  the  de- 
scription of  symptoms  to  result  from  irritation  of  the  abdominal 
viscera,  from  irritation  of  a  peripheral  nerve,  and  undoubtedly 
also  from  disturbances  within  the  pelvic  organs.  It  is  my  opinion 
that  the  same  sort  of  influences  may  excite  an  attack  of  palpita- 
tion instead  of  pain.  The  same  thing  is  true,  I  believe,  as  regards 
the  impressions  which  are  said  to  arouse  an  attack  of  pseudo- 
angina  through  the  vaso-motor  centres.  Palpitation  of  this  origin 
is  not  common,  however,  any  more  than  is  pure  vaso-motor  pseudo- 


724:  DISEASES  OF  THE  HEART 

angina.  Instances  in  which  an  attack  of  pain  is  called  forth  by 
washing  the  hands  in  too  cold  water  or  by  the  impression  made 
by  a  cold  wind  n])on  the  intercostal  nerves  are  certainly  excep- 
tional. Of  the  toxic  agencies  accredited  with  the  production  of 
pseudo-angina  pectoris,  disordered  action  of  the  heart,  prsecordial 
anxiety,  oppression,  etc.,  tobacco  is  by  far  the  most  frequent. 
This  influence  of  the  weed  is  not  very  common,  and  yet  I  have 
under  observation  at  the  present  time  a  gentleman  wdio  assures 
me  that  he  cannot  smoke  a  single  pipeful  of  mild  tobacco  without 
feeling  his  heart  beat  more  rapidly  and  strongly  than  ordinary. 

Diagnosis. — In  deciding  the  question  whether  or  not  a  pa- 
tient's symptoms  warrant  their  being  classified  as  a  cardiac  neu- 
rosis, one  should  bear  in  mind  that  they  are  independent  of  struc- 
tural alteration  of  the  heart,  and  are  in  reality  one  of  the  mani- 
festations of  a  disordered  nervous  system.  Consequently  one 
must  first  seek  in  the  personal  and  family  history  and  by  a  care- 
ful analysis  of  the  symptoms  for  evidence  of  hysteria,  neuras- 
thenia, or  of  a  highly  neurotic  temperament,  conditions  which 
have  been  shown  to  possess  an  etiologic  influence  over  the  phenom- 
ena that  form  a  clinical  picture  of  cardiac  neurosis. 

This  being  so  far  as  possible  settled,  it  is  next  necessary  to 
determine  the  presence  or  absence  of  organic  heart-disease.  If 
such  can  be  excluded,  and  the  patient  belongs  to  the  age  and  sex  in 
which  neuroses  are  most  prevalent,  a  correct  diagnosis  cannot  for 
the  most  part  be  difficult.  If,  on  the  contrary,  structural  altera- 
tion of  the  heart  is  detected,  or  if  the  patient  has  arrived  at  the 
time  of  life  wdien  myocardial  degeneration  is  likely,  then  one 
should  be  most  cautious  about  expressing  a  positive  opinion.  It  is 
very  possible  that  he  has  to  do  with  a  case  in  which  there  is  a 
blending  of  neurosis  with  structural  cardiac  disease.  In  all  in- 
stances, even  in  the  young,  one  must  carefully  study  the  nature 
of  the  symptoms,  carefully  discriminating  those  pointing  to  insta- 
bility of  the  nervous  system  from  such  as  indicate  cardiac  as- 
thenia. One  should  therefore  inquire  minutely  concerning  the 
effect  of  exercise,  for  although  one  cannot  assert  positively  that 
physical  effort  is  without  influence  upon  symptoms  in  cardiac 
neuroses,  still  such  is  ordinarily  the  case.  This  applies  as  well 
to  anomalies  of  cardiac  action  as  to  the  differential  diagnosis  of 
pseudo-angina. 


FUNCTIONAL  DISORDERS  T25 

Furthermore,  without  wishing  to  set  it  down  as  an  infallible 
guide,  1  desire  to  give  it  as  the  result  of  years  of  observation  that, 
if  the  patient  is  not  subjectively  aware  of  disorders  of  his  cardiac 
rhythm,  there  is  probably  myocardial  disease  even  if  objective 
proof  of  the  same  cannot  be  had.  The  reverse  does  not  obtain. 
The  matter  of  dyspnea  requires  close  study.  Patients  with  car- 
diac inadequacy  from  whatever  cause  experience  shortness  of 
breath  upon  exertion  and  not  during  repose  except  in  an  advanced 
stage.  Neurotic  individuals,  on  the  contrary,  unless  markedly 
neurasthenic,  are  able  to  walk  without  breathlessness,  whereas 
they  are  very  apt  to  complain  that  they  are  unable  to  draw  a  long 
breath,  or  that  they  feel  a  "  catch  in  their  breath."  They  breathe 
superficially,  and  every  now  and  then  take  an  unusually  deep  in- 
spiration, which  is  followed  by  a  feeling  of  great  relief. 

If  one  is  summoned  hastily  to  administer  relief  to  a  patient  in 
an  attack  of  palpitation,  a  sinking  spell,  etc.,  a  correct  diagnosis 
is  not  always  easy  at  first.  Valuable  information  may  be  obtained, 
however,  from  inquiry  into  the  history  as  regards  previous  at- 
tacks, mode  of  onset,  etc.,  and  from  attention  to  the  absence  of 
signs  of  organic  heart-disease  and  of  secondary  stasis.  Further- 
more, the  patient  generally  displays  nervous  agitation,  fright,  etc. 

In  those  cases  of  palpitation  which  manifest  throbbing  of  the 
aorta  either  in  the  episternal  notch  or  in  the  epigastrium,  the  dif- 
ferential diagnosis  from  aneurysm  may  be  made  by  attention  to 
the  following  points:  (1)  The  history  of  attacks  of  palpitation 
and  their  association  with  symptoms  of  neurasthenia  or  hysteria ; 
(2)  the  age  and  sex  of  the  patient,  who  is  generally  young  and 
more  often  a  female;  (3)  the  absence  of  pain,  of  signs  and  symp- 
toms of  pressure,  of  a  localized  tumour  having  an  expansile  pulsa- 
tion and  thrill;  (4)  the  absence  of  an  area  of  dulness  upon  the 
manubrium  sterni  or  at  either  side,  or  at  some  point  along  the 
course  of  the  abdominal  aorta;  (5)  the  failure  to  detect  the  aus- 
cultatory phenomena,  of  bruit  and  accentuation  of  the  vascular 
sounds  usually  present  in  aneurysm;  (6)  the  evidence  derived 
from  the  sphygmograph  and  the  X-ray. 

In  determining  the  significance  and  nature  of  pain  in  the  car- 
diac region  one  should  meet  with  but  little  difficulty  if  he  remem- 
bers the  following  points:  (1)  The  absence  in  neurotic  cases  of 
signs  of  structural  cardiac  disease ;  (2)  the  spontaneous  origin  of 


726  DISEASES  OP  THE  HEART 

the  pain,  independent  of  exercise  or  of  any  other  evidently  excit- 
ing cansc;  (3)  the  presence  of  painful  areas  in  the  course  of  the 
fourth  and  tifth  intercostal  nerves,  sliOAvn  by  Head  to  be  symp- 
tomatic of  both  functional  and  organic  disorders  of  the  stomach. 
These  hypersesthetic  zones  are  generally  found  on  the  left  side  as 
follows:  (A)  near  the  left  nipple,  upon  the  fifth  rib,  or  in  the  in- 
terspace immediately  above  or  below;  (B)  another  upon  the 
fourth  costal  cartilage  or  in  the  fourth  interspace  near  the  ster- 
num;  (C)  at  the  lower  end  of  the  sternum  or  upon  its  appendix. 
There  are  frequently  other  painful  points  upon  the  back  near  the 
inferior  angle  of  the  scapula.  The  tender  areas  symptomatic  of 
disorders  of  the  thoracic  organs  are,  according  to  the  same  author, 
located  higher  up,  being  in  front  on  the  sternum  near  the  level  of 
the  third  costal  cartilage,  and  on  the  third  rib,  or  near  by,  just 
within  the  vertical  mamillary  line.  When  the  tender  points  first 
mentioned  are  discovered  close  inquiry  will  usiially  elicit  symp- 
toms of  indigestion  or  the  so-called  auto-infection. 

For  the  most  part  the  correct  diagnosis  of  the  pseudo-anginas 
is  difficult  only  in  patients  at  or  after  middle  age,  and  in  them 
the  question  is  likely  to  be  rendered  still  more  difficult  by  the  dis- 
covery of  cardiac  hypertrophy  or  arterial  thickening.  In  such  an 
event  a  positive  diagnosis  must  often  be  deferred  until  time 
throws  further  light  on  the  case.  In  most  cases,  however,  a  cor- 
rect diagnosis  is  possible  by  the  discovery:  (1)  That  the  attacks, 
as  previously  mentioned,  arise  independent  of,  and  are  as  a  rule 
iminfluenced  by,  physical  effort;  (2)  the  suiferer  is  not  compelled 
to  seek  the  erect  posture,  but  frequently  prefers  to  lie  down;  (3) 
he  does  not  present  a  picture  of  silent  motionless  agony,  but  moans 
or  cries  aloud  and  moves  about  restlessly;  (4)  the  attack  is  of 
much  longer  duration,  often  lasting  several  hours;  (5)  it  is  often 
[)ossible  to  discover  signs  of  peripheral  disease  that  may  exert  a 
reflex  influence  or  to  get  a  history  of  influences  that  are  operable 
through  the  vaso-motor  system  or  act  as  a  toxin.  As  regards  tobac- 
co, however,  it  should  be  needless  to  suggest  that  in  middle-aged 
men  who  are  smokers  coronary  sclerosis  is  much  more  likely  to  be 
the  cause  than  is  their  tobacco. 

Prognosis. — I'his  is  practically  that  of  the  underlying  neu- 
rosis. These  cases  are  often  of  very  long  standing,  and  therefore 
present  a  correspondingly  unfavourable  prospect  of  cure.     In  the 


FUNCTIONAL   DISORDERS  727 

young,  when  the  case  is  unmistakably  one  of  neurosis,  the  assur- 
ance can  unhesitatingly  be  given  that  death  will  not  result  from 
the  attack  of  palpitation  or  pseudo-angina.  When  the  diagnosis  is 
doubtful,  the  patient  may,  for  the  moral  effect,  be  told  that  his 
cardiac  symptoms  are  functional,  yet  the  friends  should  be 
warned  of  the  possibly  grave  nature  of  the  case.  In  strictly  neu- 
rotic subjects  the  prognosis  depends,  moreover,  upon  the  possi- 
bility of  the  removal  of  all  those  influences  of  environment  which 
unfavourably  affect  the  patient.  In  Graves's  disease,  or  those 
allied  states  associated  with  enteroptosis,  the  prospect  of  obtaining 
immunity  from  their  tachycardia  and  palpitations  is  very  un- 
promising. . 

Treatment. — This  must  be  directed  not  alone  to  the  relief  of 
the  j)aroxysms  of  palpitation  or  pain,  but  also  to  the  removal  if 
possible  of  the  underlying  neurosis.  It  is  not  the  province  of  this 
work  to  discuss  the  management  of  neurasthenia  and  hysteria, 
and  therefore  the  reader  is  referred  to  works  dealing  with  the  sub- 
ject. It  need  only  be  remarked  here  that  the  physician  who  would 
successfully  treat  cardiac  neuroses  must  command  the  entire  con- 
fidence and  respect  of  his  patient,  and  he  must  use  the  influence 
thus  gained  for  their  proper  moral  management.  He  must  dis- 
play no  hesitation  or  vacillation  in  his  suggestions  and  no  irreso- 
lution in  their  enforcement. 

Treatment  of  the  Attack. — In  most  instances  the  medical  at- 
tendant first  sees  the  patient  in  one  of  his  seizures,  and  is  there- 
fore called  on  to  act  energetically  and  promptly.  Yet  he  should 
never  be  in  such  haste  that  he  cannot  first  gain  a  tolerably  correct 
notion  of  the  nature  of  the  disorder.  He  should  never  display 
alarm,  and  even  if  he  thinks  so,  he  should  never  tell  the  patient  he 
is  in  danger  of  dying.  On  the  contrary,  he  should  endeavour  to 
reassure  the  patient  both  by  word  and  the  calmness  of  his  manner. 
Whether  the  attack  is  one  of  palpitation  merely,  or  one  of  intense 
pain,  the  treatment  is  essentially  the  same,  for  there  are  usually 
associated  symptoms  of  vaso-motor  disturbance. 

Palpitation. — I  have  never  been  able  to  see  the  wisdom  of  re- 
sorting to  digitalis  or  remedies  of  similar  action  for  the  arrest  of 
an  attack  of  palpitation.  These  remedies  are  slow  of  action,  the 
attack  is  in  most  instances  short-lived,  and  before  the  digitalis 
takes  effect  the  tumultuous  heart-action  subsides  spontaneously,  or 


728  DISEASES  OF  THE  HEART 

because  some  other  measure  has  met  tlic  indication.  If  there 
are  pallor  of  the  countenance,  coldness  of  the  extremities,  and  a 
small  contracted  pulse,  a  rapidly  diffusible  stimulant  is  indicated. 
The  arterioles  should  be  dilated  so  as  to  cause  warmth  and  flush- 
ing of  the  surface,  even  though  the  pulse  be  rapid  as  well  as  small. 
To  this  end  nitroglycerin  is  efficient  and  usually  affords  prompt 
relief.  It  is  better  to  dissolve  a  tablet  or  to  drop  a  minim  of  a 
1-per-cent  solution  on  the  tongue,  for  its  action  is  more  prompt 
than  when  swallowed.  Whisky,  ammonia,  camphor,  or  even  hot 
ginger  tea  or  hot  peppermint  water  may  be  given,  while  heat 
should  also  be  applied  to  the  extremities  and  prsecordium.  If  in- 
stead of  being  cold  the  surface  of  the  body  is  warm  and  the  face 
flushed,  pulse  full  and  bounding^  then  diffusible  stimulants  are 
contra-indicated.  It  is  now  better  to  apply  ice  to  the  pra^cordium 
and  to  give  a  full  dose  of  one  of  the  bromides,  with  possibly  2  or  3 
drops  of  tincture  of  aconite  root.  This  may  be  followed  by  a  dose 
of  digitalis  or  strophanthus.  In  most  cases  fear  plays  an  impor- 
tant part  in  maintaining  the  attack,  and  consequently  the  very 
presence  of  the  doctor,  provided  his  manner  is  calm  and  reassur- 
ing, will  do  much  to  aid  the  action  of  remedies.  If  the  seizure  is 
unusually  refractory  and  the  patient's  agitation  does  not  subside 
after  a  sufficiently  long  trial  of  the  line  of  treatment  indicated 
above,  then  it  may  be  well  to  inject  ^  of  a  grain  of  morphine  for 
its  calmative  effect. 

The  Attach  of  Pain. — If  the  pra:'Cordial  distress  is  not  suffi- 
cient to  merit  the  term  of  pseudo-angina,  l)eing  plainly  a  pleuro- 
dynia with  cardiac  anxiety,  it  may  yield  to  the  application  of  a 
sinapism  or  of  simple  heat  to  the  chest.  If  there  are  signs  of 
vaso-motor  spasm,  or  if  the  pulse  is  weak  and  perhaps  slow  and 
irregular  or  intermittent,  a  rapidly  acting  stimulant  of  the  kind 
mentioned  above  should  be  given. 

If  the  paroxysm  is  a  pseudo-angina  either  one  of  two  remedies 
is  indicated :  nitroglycerin  where  there  is  arterial  spasm,  and 
m(irj)hine  subcutaneously  where  there  is  or  is  not  such  spasm. 
This  latter  not  only  allays  pain  and  acts  as  an  efficient  cardiac 
stimulant,  but  it  calms  the  patient  and  promotes  subsequent  sleep. 
Nevertheless  it  is  well  to  bear  in  mind  that  there  is  always  danger 
of  these  neurotic  patients,  wlio  suffer  from  fi-ccpient  attacks  of 
l)ain,  learning  to  depend  ujion  the  drug,  and  thus  in  time  becom- 


FUNCTfONAL  DISORDERS  729 

ing  victims  of  the  morphine  habit.  The  same  objection  applies  to 
the  use  of  alcoholic  stimulants  for  the  treatment  of  an  attack  of 
palpitation,  sinking  spells,  etc.,  and  therefore  it  is  better  to  rely 
on  other  harmless  but  equally  effective  stimulants. 

In  conclusion,  the  physician  should  search  for  and  endeavour 
to  remove  all  those  sources  of  visceral  or  perij^heral  irritation 
which  serve  to  disturb  the  nervous  system  between  attacks  or  may 
seem  to  act  as  exciting  causes. 

Enteroptosis,  dilatation  of  the  stomach,  digestive  indiscre- 
tions, or  any  other  condition  that  may  account  for  the  cardiac 
symptoms  are  to  be  treated  in  accordance  with  the  principles  ap- 
plicable to  such  cases  and  the  special  indications  of  each  case. 
Great  amelioration  and  sometimes  entire  relief  of  the  distressing 
attacks  of  palpitation  follow  so  simple  a  measure  as  the  wearing 
of  a  properly  fitted  abdominal  supporter  in  cases  of  ptosis  of  the 
stomach  or  other  viscera.  In  addition,  attention  must  be  paid  to 
the  clothing,  that  too  tight  skirt-bands  or  corsets  may  not  in- 
crease the  dragging  of  the  abdominal  contents  upon  their  sup- 
ports. Properly  given,  massage  is  often  of  much  benefit  in  these 
cases. 

Finally,  in  all  cases  the  exciting  causes  should  be  carefully 
sought  out  and  the  patient  impressed  with  the  necessity  of  avoid- 
ing all  those  influences  which  may  precipitate  an  attack.  He 
should  be  told  that  if  he  is  to  get  better  he  is  to  aid  in  his  cure  by 
obeying  instructions  to  the  letter,  since  medicines  alone  are  in- 
capable of  eradicating  his  disorder. 


CHAPTER    XXXI 
ESSENTIAL    PAROXYSMAL    TACHYCARDIA 

This  is  a  highly  interesting  and  very  puzzling  derangement 
of  the  heart's  action  which  has  received  much  attention  from  the 
medical  profession  since  1867,  the  date,  according  to  Herringham, 
of  the  publication  by  Payne  Cotton  of  the  first  recorded  case. 
This  disorder  of  cardiac  rhythm  consists  in  exceeding  rapidity  of 
action,  and  occurs  in  attacks  of  variable  duratioxi  and  frequency, 
during  which  the  heart-beats  number  160  or  more  to  the  minute. 
]\Iedical  men  in  the  British  Isles  have  always  been  keen  observers, 
and  here  again,  as  in  angina  pectoris  and  bradycardia,  have  sig- 
nalized their  powers  of  observation.  Cotton,  Edmunds,  Watson, 
and  Bowles  led  the  way,  and  in  the  next  few  years  other  observa- 
tions were  recorded  by  Nunnely,  Cavafy,  and  Farquharson.  On 
the  Continent  we  find  the  names  of  Tuchzek,  Gerhardt,  Bouveret, 
Oettinger,  Probsting,  and  many  others.  Gerhardt  suggested  the 
term  Tachycardia  in  the  year  1881,  and  in  1888  Bouveret  sug- 
gested the  appellation  Essential  Paroxysmal  Tachycardia,  to  dis- 
tinguish cases  in  which  the  paroxysms  of  excessively  rapid  action 
furnished  the  only  clinical  evidence  of  cardiac  disease. 

Acceleration  of  the  heart's  action  to  140,  150,  and  even  to  170 
in  the  minute  is  sometimes  observed  in  cases  of  valvular  lesion, 
and  may  be  assumed  to  depend  in  some  way  upon  structural  alter- 
ation of  the  walls  due  to  the  valve  defect.  But  in  those  cases 
which  Bouveret  characterizes  as  essential  tachycardia  there  is  no 
clinical  evidence  of  cardiac  disease,  and  therefore  tlio  ])arnxysms 
cannot  be  considered  symptomatic.  This  distinction  is  objected 
to,  however,  by  Herringham,  Gibson,  and  others,  who  prefer  to 
call  the  condition  simply  paroxysmal  tachycardia,  since  this  ap- 
plies broadly  to  all  cases  in  which  typical  attacks  of  excessively 
rapid  action  occur. 
730 


ESSENTIAL  PAROXYSMAL  TACHYCARDIA  Y31 

Clifford  Allbiitt  objects  to  the  term  paroxysmal,  saying,  "  The 
interpretation  is  that  tachycardia  is  a  fairly  uniform  symptom 
groii}) ;  and,  as  one  of  its  eminent  characters  is  its  paroxysmal 
occurrence,  the  addition  of  this  qualification  to  the  name  is  super- 
fluous." 

Pathology. — There  are  no  anatomical  changes  that  can  be 
definitely  associated  with  essential  paroxysmal  tachycardia,  and 
likewise  there  is  no  established  pathological  basis  upon  which  an 
explanation  of  the  phenomenon  may  rest.  Prior  to  1897  six  post- 
mortem observations  had  been  made  in  this  class  of  cases,  but 
they  failed  to  disclose  any  constant  or  uniform  lesion.  In  one, 
the  wall  of  the  left  ventricle  was  in  a  state  of  pronounced  fibrous 
degeneration,  and  in  two  the  hearts  were  extensively  fatty,  while 
in  three  others  no  special  changes  were  noted  aside  from  dilata- 
tion. As  these  alterations  have  been  found  over  and  over  again, 
indeed,  are  very  common  in  hearts  that  have  never  manifested  this 
peculiar  disorder  of  action,  it  is  plain  that  there  is  nothing  in 
these  post-mortem  findings  to  explain  the  occurrence  of  parox- 
ysmal tachycardia.  Consequently  various  theories  have  been 
offered  to  account  for  the  attacks. 

Tuchzek  suggested  paralysis  of  the  vagus,  and  IS^othnagel,  irri- 
tation of  the  sympathetic,  sufficient  to  overcome  the  controlling 
influence  of  the  pneumogastric.  It  has  also  been  suggested  that 
there  may  be  a  combined  action  of  the  two,  vagus  paresis  and  ac- 
celerator stimulation.  Objections  are  urged  against  all  of  these 
theories.  Tuchzek's  theory  has  been  widely  accepted,  and  yet  ex- 
periments on  animals  have  failed  to  produce  so  extreme  a  rapidity 
of  heart-action  as  is  seen  in  these  attacks,  and  Allbutt  believes 
that  in  man  abeyance  of  the  inhibitory  control  of  the  vagus  would 
not  send  the  pulse  up  beyond  120.  Likewise,  stimulation  of  the 
cardiac  accelerator  nerve  is  said  not  to  increase  the  pulse-rate 
beyond  150.  Ascribing  the  rapid  action  to  a  combination  of  both 
necessitates  the  assumption  of  some  cause  which  acts  simultane- 
ously on  both  nerves,  and  this,  in  Allbutt's  emphatic  words,  "  sins 
against  the  economy  of  causes." 

Bouveret's  suggestion  that  it  is  a  bulbo-spinal  neurosis,  and 
Talamon's  that  it  is  of  an  epilpetic  nature,  are  both  not  acceptable. 
Samuel  West  has  urged  that  the  attacks  are  due  to  alterations  in 
the  myocardium,  to  which  Herringham  would  add  changes  in  the 


732  DISEASES  OP  THE  HEART 

nerve  endings  situated  in  the  heart,  a  view  that  seems  to  appeal 
strongly  to  Gibson.  Other  suggestions,  as  a  neuritis,  are  of  still 
less  importance.  They  are  all  mere  surmises ;  and  in  the  present 
state  of  our  knowledge,  without  numerous  and  careful  necropsies 
to  throw  light  on  the  anatomical  changes  underlying  this  interest- 
ing symptom  or  disease,  whichever  it  may  be,  we  can  only  say 
witli  posit iveness  that  we  know  nothing  concerning  its  true  nature. 

Etiology. — This  is  likewise  obscure.  Most  of  the  recorded 
cases  have  been  in  adults.  Of  the  53  cases  collected  by  Herring- 
ham,  the  age  was  stated  in  40,  and  of  these  there  were  7  instances 
in  children,  12  between  the  ages  of  twenty  and  thirty,  and  13  in 
the  following  decade  of  life,  the  remainder  being  in  persons  past 
forty.  Age,  therefore,  cannot  be  said  to  exert  special  predispos- 
ing influence.  Both  sexes  are  subject  to  attacks,  and  although  30 
of  Herring-ham's  collected  instances  were  in  males,  the  prepon- 
derance of  this  sex  is  so  slight  that  it  scarcely  warrants  the  con- 
clusion that  in  sex  alone  resides  any  predisposing  influence. 

That  in  some  cases  there  may  be  an  hereditary  element  ap- 
pears to  be  established  by  Oettinger's  case,  since  there  was  history 
of  the  same  sort  of  attacks  in  three  preceding  generations.  In  some 
of  the  reported  cases  there  has  been  a  history  of  previous  disease 
— rheumatism,  influenza,  diphtheria,  malaria,  amemia — that  may 
possibly  have  been  a  predisposing  factor,  but  a  definite  relationship 
of  this  kind  has  not  been  established. 

In  the  way  of  possible  exciting  causes  have  been  a  blow  on 
the  chest,  fright  or  other  strong  emotion,  and  a  sudden  physi- 
cal effort.  Attacks  have  also  followed  disturbances  in  the  digest- 
ive tract. 

Komberg  states  that  paroxysmal  tachycardia  rests  on  a  nerv- 
ous basis,  and  may  arise  reflexly  from  disorder  in  any  of  the  vis- 
cera or  may  result  from  some  cause  acting  directly  througli  the 
central  nervous  system,  and  is  independent  of  any  demonstrable 
cardiac  disease.  Thus  it  is  plain  that  after  all  has  been  written 
on  the  subject  of  its  pathogenesis  we  are  no  wiser  than  we  were 
before. 

Features  of  the  Paroxysm. — Two  conditions  are  essential  if 
rapid  action  of  the  heart  is  to  be  considered  an  instance  of  essen- 
tial paroxysmal  tachycardia:  (1)  Tlie  apparently  healthy  heart 
must  beat  at  least  100  times  a  minute.     (2)    The  onset  and  ter- 


ESSENTIAL  PAROXYSMAL  TACHYCARDIA  733 

minatiou  of  the  attack  must  be  so  sudden  and  abrupt  as  to  give  it 
the  character  of  a  paroxysm.  Although  a  pulse-rate  of  less  than 
160  is  frequently  observed  in  persons  with  some  structural  disease 
of  the  heart,  still  in  essential  tachycardia  the  number  of  cardiac 
contractions  is  often  vastly  in  excess  of  this  number,  running  as 
high  as  200,  and  in  a  few  instances  even  to  300  a  minute.  The 
pulse  is  small,  thready,  and  often  uncountable,  because  the  ex- 
treme frequency  of  the  waves  and  the  emptiness  of  the  vessel 
cause  the  pulse-waves  to  run  together  in  an  indistinguishable 
manner.  To  determine  the  heart-rate,  therefore,  one  must  count 
the  heart-beats  by  auscultation  instead  of  by  palpating  a  periph- 
eral artery. 

The  rhythm  of  the  contractions  is  usually  regular,  but  irregu- 
larity and  inequality  in  their  force  are  sometimes  observed.  The 
extreme  rapidity  of  the  cardiac  systoles  is  at  the  expense  of  their 


Fig.  108. — Sphtgmogram  from  Case  of  Paeoxysmal  Tachtcaedia. 

Strength  and  efficiency,  blood-waves  of  normal  volume  are  not  dis- 
charged into  the  aorta,  the  arterial  system  becomes  relatively 
empty,  and  the  pulse  is  one  of  strikingly  low  pressure.  This  is 
illustrated  by  the  appended  tracing  (Fig.  108)  kindly  furnished 
me  by  Dr.  E.  F.  Wells  from  one  of  his  cases. 

The  paroxysms  begin  abruptly  and  generally  without  premoni- 
tion. Indeed,  upon  the  occurrence  of  the  first  attack  the  patient 
does  not  always  know  what  is  the  matter  with  him,  and  is  only 
able  to  say  he  feels  bad.  If  the  tachycardia  is  short  lived,  the 
patient  may  experience  nothing  more  than  a  vague  feeling  of  dis- 
comfort and  his  outward  appearance  may  not  disclose  anything 
unusual  to  the  ordinary  observer.  There  may  be,  however,  pallor 
or  flushing  of  the  countenance.  In  some  instances  there  are  pra3- 
cordial  oppression  and  even  pain,  numbness  or  tingling  of  the  arm 
(Gibson).  Palpitation  or  fluttering  of  the  heart  may  be  com- 
plained of,  and  vertigo  is  sometimes  experienced.  Most  sufferers 
from  this  complaint,  notwithstanding  repeated  attacks  and  the 


734  DISEASES  OF  THE  HEART 

fact  that  experience  has  shown  the  termination  to  be  in  sudden 
recovery,  become  greatly  alarmed,  and  if  the  attack  is  prolonged 
to  several  days  fall  into  a  state  of  great  mental  and  physical  dis- 
tress. 

If  the  case  is  seen  early  there  is  usually  so  little  evidence  of 
the  actual  state  of  things  in  the  patient's  outward  appearance  that 
the  medical  attendant  on  feeling  the  radial  pulse  is  usually  struck 
with  astonishment  and  even  dismay  at  its  rapidity. 

If  the  attack  lasts  long  enough  it  leads  to  cardiac  inadequacy 
and  the  blood  tends  to  accumulate  in  the  heart-cavities.  The  heart 
becomes  overdistended  and  the  venous  side  of  the  circulation  en- 
gorged, as  shown  by  increased  cardiac  dulness,  cyanosis,  and  it 
may  be  by  pulsation  of  the  jugulars  (Gibson).  There  is  pulmo- 
nary congestion,  possibly  also  a  small  amount  of  oedema,  and  even 
albuminuria.  The  heart-sounds  are  feeble  and  the  first  at  the 
apex  may  become  almost  inaudible. 

In  most  cases  the  duration  of  the  paroxysm  is  not  sufficient 
to  lead  to  such  marked  signs  of  stasis.  The  attack  subsides  sud- 
denly after  a  few  hours  and  the  patient  is  left  very  much  as  he 
was  before,  feeling  perhaps  tired  and  dreading  a  recurrence,  but 
able  to  return  to  his  ordinary  duties. 

A  striking  peculiarity  of  such  a  paroxysm,  whether  long  or 
short,  is  the  persistence  of  the  tachycardia  even  during  sleep. 
Such  attacks  are  usually  repeated  through  a  series  of  years,  and 
yet  cases  have  been  observed  in  which  but  a  single  paroxysm  was 
noted.  Although  recurrences  are  the  rule,  there  is  no  regularity 
in  their  repetition. 

Their  duration  is  likewise  variable,  since  the  paroxysms  may 
last  from  a  few  minutes  to  one  or  more  days.  In  one  or  two  in- 
stances the  tachycardia  persisted  for  two  or  even  three  weeks. 

If  the  tachycardia  is  a  symptom  of  some  visceral  disturbance, 
or,  in  other  words,  is  a  functional  derangement  of  reflex  origin, 
then  it  is  easy  to  conceive  of  but  a  single  attack  and  to  understand 
how  this  may  be  of  short  duration.  But,  if  it  is  due  to  some  deli- 
cate and  as  yet  unrecognisable  alteration  in  the  myocardium  or 
bulb,  then  recurrences  should  be  the  rule,  as  indeed  they  are,  and 
the  nttar-ks  slionld  be  of  considerable  duration. 

Diagnosis. — The  determination  of  the  fact  of  tachycardia 
is  not  difficult.     The  point  to  be  decided  is  whether  the  rapid  ac- 


ESSENTIAL  PAROXYSMAL  TACHYCARDIA  735 

tion  is  an  instance  of  essential  paroxysmal  tachycardia  or  is  of  the 
kind  called  symptomatic.  If  it  belongs  to  the  former  class,  it 
should  fulfil  the  following  requirements:  (1)  A  heart-rate  for  the 
time  being  of  at  least  160  a  minute,  (2)  abruptness  of  onset  and 
equal  suddenness  of  termination,  (3)  failure  to  detect  evidence  of 
heart-disease  either  during  or  between  attacks. 

If,  on  the  other  hand,  there  is  evidence  of  myocardial  or  endo- 
cardial disease,  the  tachycardia  is  symptomatic  and  not  essential, 
no  matter  how  rapid  may  be  the  pulse.  In  this  class,  however,  it 
is  not  usual  for  the  heart's  action  to  exceed  150  a  minute.  Most 
instances  of  "  heart  hurry  "  belong  to  this  class,  and  yet  it  is  prob- 
able that  the  essential  form  occurs  more  often  than  is  reported, 
either  because  the  attacks  come  to  the  notice  of  the  family  doctor 
rather  than  of  the  consultant,  or  because  the  attacks  are  so  tran- 
sient that  no  physician  is  called  in.  Although  I  have  repeatedly 
observed  symptomatic  tachycardia  and  have  known  several  indi- 
viduals who  gave  a  history  of  the  essential  form,  among  them  a 
medical  man,  I  have  not  actually  v^itnessed  a  paroxysm. 

Prognosis. — In  the  essential  form  the  prognosis  may  be 
said  to  be  favourable  so  far  as  life  is  concerned.  There  is  always 
an  element  of  uncertainty  in  any  case  of  extreme  and  protracted 
"  heart  hurry,"  but  if  a  paroxysm  terminates  speedily  no  damage 
to  the  heart  may  be  sustained.  The  real  difficulty  lies  in  the 
uncertainty  of  the  length  of  time  during  which  an  attack  may 
endure.  In  the  aged,  the  feeble,  and  persons  having  a  definite 
cardiac  lesion  such  paroxysms  are.  not  devoid  of  danger.  In 
most  cases  of  paroxysmal  tachycardia  the  seizure  may  be  expected 
to  terminate  abruptly  and  spontaneously,  but  how  long  the  patient 
is  to  remain  immune  from  a  repetition  is  a  matter  of  too  much 
uncertainty  for  the  prudent  physician  to  express  an  opinion.  The 
history  of  cases  shows  that  in  most  instances  other  attacks  are  to 
be  expected. 

Treatment. — The  plain  indication  is  if  possible  to  arrest 
the  paroxysm.  This  is  called  for,  notwithstanding  the  fact  that  in 
the  majority  of  cases  the  tachycardia  has  not  caused  death.  Al- 
though a  patient  may  have  had  repeated  attacks  that  have  ceased 
spontaneously,  yet  tachycardia  is  such  an  uncertain  quantity  that 
one  can  never  be  quite  sure  how^  another  paroxysm  may  affect  the 
heart.    Unfortunately  it  is  the  same  with  this  as  with  other  mala- 


736  DISEASES  OF  THE  HEART 

dies;  our  therapeutic  resources  do  not  always  enable  us  to  meet 
indications  satisfactorily. 

Theoretically,  digitalis  ought  to  enable  us  to  slow  down  a  run- 
aw^ay  heart,  but  experience  has  shown  its  inefficiency  in  most  cases. 
This  remedy  should  not  be  administered  recklessly  in  paroxysmal 
tachycardia,  for  if  the  attacks  were  to  terminate  spontaneously 
soon  after  the  administration  of  a  single  very  large  dose  or  of 
several  massive  ones  in  quick  succession,  there  might  be  positive 
danger  of  poisonous  effects.  If,  as  stated  by  Allbutt,  digitalis 
produces  diuresis  even  when  it  does  not  control  the  heart's  action, 
it  is  likely  to  be  eliminated  and  evil  consequences  will  not  result. 
Nevertheless,  it  is  well  not  to  administer  more  than  10  minims  of 
the  tincture  hourly  for  six  hours,  and  if  at  the  end  of  this  time 
no  appreciable  slowing  of  the  pulse  is  produced,  to  have  recourse 
to  other  means. 

Ice  may  be  applied  to  the  praecordia,  or  one  may  try  the  effect 
of  prolonged  but  not  too  vigorous  friction  of  the  skin  over  the 
upper  portion  of  the  spinal  column,  which  has  been  said  to  slow 
the  heart.  The  vagus  may  be  compressed  in  the  neck,  or  it  may 
be  stimulated  by  an  electric  current. 

It  has  also  been  recommended  that  the  patient  take  a  deep 
inspiration,  and  then  with  his  arms  folded  across  the  front  of  the 
chest  and  his  feet  pressed  firmly  against  the  foot-board  of  the  bed 
to  make  a  powerful  expiratory  effort  while  the  glottis  is  kept 
closed.  One  of  my  patients  who  is  a  sufferer  from  essential 
paroxysmal  tachycardia  assures  me  that  she  has  sometimes  been 
able  to  check  her  heart  by  drawing  a  full  breath,  then  w^hile  her 
body  is  flexed  so  as  to  compress  her  abdomen,  making  a  powerful 
expiratory  pressure.  In  her  case  also  a  paroxysm  has  been  known 
to  be  arrested  by  the  pouring  of  cold  water  over  her  wrists. 

Whatever  remedy  is  administered  or  wdiatev^r  method  of  im- 
pressing the  nervous  system  is  tried,  it  is  often  found  useless.  It 
then  becomes  the  physician's  duty  to  support  the  heart  until  the 
tachycardia  subsides  spontaneously,  and  when  cardiac  dilatation 
sets  in,  this  is  imperative.  To  this  end  reliance  must  be  placed 
on  strychnine,  caffeine,  digitalis,  etc.,  while  the  patient  is  kept  at 
rest.  The  diet  is  to  be  simple  and  nourishing,  and  tea,  coffee,  or 
other  stimulants  are  to  be  forbidden.  In  prolonged  attacks  it  may 
be  well  also  to  administer  a  "ontle  cathartic. 


ESSENTIAL  PAROXYSMAL  TACHYCARDIA  737 

It  may  not  bo  possible  to  prevent  recurrences,  and  attempts  in 
that  direction  may  seem  to  be  somethiilg  like  firing  in  the  dark, 
yet  the  patient  should  receive  medical  attention  between  attacks. 
In  cases  exhibiting  subsequent  signs  of  cardiac  strain  or  in  which 
there  is  an  unstable  nervous  system,  such  regular  treatment  is  spe- 
cially advisable.  Gibson  recommends  tonics,  a  course  of  the  ITau- 
heim  baths  with  resistance  gymnastics  and  such  other  measures  as 
the  experience  of  the  medical  attendant  and  the  exigencies  of  each 
case  suggests.  In  some  instances  it  may  be  well  to  give  digitalis 
or  other  heart-tonics  for  a  long  time.  Every  effort  should  be  made 
to  discover  and  remove  any  source  of  reflex  irritation,  and  the 
daily  life  should  be  as  healthful  and  free  from  excitement  as 
possible. 


48 


SECTION  V 
DISEASES  OF  THE  ARTERIAL  SYSTEM 


CHAPTER    XXXII 
ARTERIOSCLEROSIS 

Degenerative  changes  in  the  coats  of  the  blood-vessels  were 
observed  as  long  ago  as  the  days  of  Senac  and  Morgagni,  and  by 
these  investigators  were  described  as  an  inflammatory  process. 
It  is  to  Rokitansky  and  Virchow,  however,  that  we  are  indebted 
for  thorough  and  systematic  investigations  concerning  the  origin 
and  nature  of  the  process  to  which  Lobstein  had  previously  given 
the  name  of  arteriosclerosis.  Virchow  regarded  it  as  a  chronic 
arteritis  and  pointed  out  its  similarity  to  the  slow  inflammatory 
process  so  often  seen  in  the  viscera,  which  is  attended  by  the  devel- 
opment of  fibrous  tissue.  The  inflammatory  nature  of  arterio- 
sclerosis was  accepted  by  other  pathologists  also,  but  by  certain 
of  them  was  regarded  as  an  evidence  of  some  infectious  process. 

On  the  other  hand,  the  cause  of  the  sclerotic  change  was  by 
Traube  and  others  found  in  mechanical  factors — i.  e.,  in  an  in- 
crease of  the  arterial  blood-pressure  following  persistent  contrac- 
tion of  the  arterioles.  Indeed,  some  went  so  far  as  to  attribute 
to  high  blood-pressure  every  case  in  which  they  recognised  sclero- 
sis and  secondary  cardiac  hypertrophy. 

The  latest  view  of  the  pathology  of  this  vascular  change  and 
the  one  that  is  coming  into  general  acceptance  is  that  of  Thoma. 
Concisely  stated,  his  conception  of  the  process  is  that  in  conse- 
quence of  lessened  resistance  of  the  media  the  vessel  becomes 
widened  with  resulting  slowing  of  the  blood-stream.  Connective 
tissue  then  develops  in  the  subendothelial  layers  of  the  intima  as  a 
compensatory  process  by  which  to  restore  the  normal  relation  be- 
738 


ARTERIOSCLEROSIS  739 

tween  the  artery  and  its  contents.  Although  in  most  instances  the 
vascular  change  is  an  attempt  to  make  good  a  loss  of  elasticity 
and  widening  of  the  artery,  still  it  may  develop  when  the  normal 
relation  between  the  vessel  and  its  contents  is  lost  by  reason  of 
decrease  in  the  volume  of  the  blood.  Romberg,  to  whom  I  am  in- 
debted for  the  historical  data  just  given,  finds  Thoma's  view 
highly  satisfactory,  since  it  seems  to  explain  the  development  of 
arteriosclerosis  in  cases  which  were  previously  unaccountable  by 
Traube's  theory.  Moreover,  it  has  been  founded  on  an  immense 
amount  of  carefully  studied  material. 

Morbid  Anatomy. — Arteriosclerosis  consists  essentially  in 
a  degeneration  of  the  media  with  secondary  compensatory  thicken- 
ing of  the  intima.  It  may  be  localized,  constituting  the  nodular 
form  of  Councilman,  or  it  may  be  diffuse.  In  the  nodular  or  cir- 
cumscribed form  whitish  or  yellowish  patches  are  scattered  along 
the  inner  surface  of  the  vessel,  which  stand  up  from  the  surround- 
ing level  and  are  of  a  rounded  contour.  In  the  diffuse  variety 
the  arterial  wall  is  stiff,  and  more  or  less  dilated,  while  on  the 
surface  of  the  intima  may  be  zones  of  nodular  thickening  and 
calcareous  or  atheromatous  patches.  In  old  persons  the  arteries 
are  stiff,  more  or  less  tortuous  and  dilated.  The  inner  surface 
presents  numerous  calcareous  plates  and  atheromatous  ulcers. 

Examined  microscopically,  the  thickening  of  the  intima  is 
found  due  to  development  of  connective  tissue  between  the  endo- 
thelium and  underlying  elastic  tissue.  After  a  time,  degenerative 
changes  take  place  in  this  newly  formed  connective  tissue  which 
consist  in  hyaline  transformation  of  the  outer  portion  with  areas 
nearer  the  endothelium  of  fine  detritus  in  which  fat  droplets  are 
seen.  These  areas  of  necrosis  constitute  the  so-called  atheroma- 
tous abscess.  When  these  areas  break  into  the  lumen  of  the  vessel 
depressions  are  left,  known  as  atheromatous  ulcers.  The  borders 
and  bottoms  of  such  ulcers  are  rough,  and  hence  may  become  the 
seat  of  white  thrombi.  By  the  deposit  of  lime  salts  in  these  ath- 
eromatous patches  calcareous  plaques  are  formed  which  project 
above  the  surface  of  the  intima,  while  by  formation  of  chalky 
particles  in  the  wall  the  artery  may  become  transformed  into  a 
tube  of  almost  bony  hardness. 

In  the  middle  coat  changes  of  a  degenerative  nature  take  place 
which  lead  to  weakening  and  dilatation  of  the  artery  and  conse- 


740  DISEASES  OF  THE  HEART 

qiient  thickening  of  the  intima.  The  middle  tunic  becomes 
thinned  in  consequence  of  atrophy  and  degeneration  of  its  muscle- 
fibres  and  of  more  or  less  extensive  destruction  of  its  elastic  ele- 
ments. In  some  cases  these  elements  disappear  entirely  and  are 
replaced  by  connective  tissue.  The  adventitia  in  its  turn  does  not 
escape,  but  becomes  infiltrated  with  round  cells,  especially  in  the 
neighbourhood  of  the  vasa  vasorum.  The  investing  membrane  be- 
comes tough  and  fibrous  and  may  also  be  of  increased  thickness. 

The  changes  of  arteriosclerosis  which  have  been  thus  briefly 
described  are  not  distributed  uniformly  in  the  afl'ected  vessel  or 
in  all  parts  of  the  arterial  system.  The  lumen  of  small  arteries 
is  apt  to  be  greatly  narrowed  and  even  obliterated  by  the  hyper- 
plasia of  their  coats,  or  it  is  blocked  by  thrombosis.  The  aorta 
and  large  arteries,  on  the  contrary,  are  apt  to  become  more  or 
less  dilated  while  their  walls  are  rigid  and  the  intima  rough  from 
the  i)resence  of  calcareous  plates  and  atheromatous  patches,  as  pre- 
viously described. 

As  already  stated,  the  various  parts  of  the  arterial  system  are 
not  equally  involved  in  the  sclerotic  process.  Thus  Bregmann 
found  as  a  result  of  analysis  of  the  cases  investigated  under 
Thoma's  direction,  that  the  ulnar  was  involved  in  94  per  cent, 
anterior  tibial  in  93,  subclavian  in  88,  cerebral  arteries  in  87,  in- 
ternal carotid  in  87,  radial  in  86,  splenic  in  82,  popliteal  in  79, 
external  carotid  in  78,  axillary  in  71,  femoral  in  69,  common  ca- 
rotid in  68,  ascending  aorta  in  67,  abdominal  aorta  in  64,  external 
iliac  in  58,  and  brachial  in  55  per  cent.  This  list  shows  some 
very  remarkable  differences  which  it  is  difficult  to  explain,  and  so 
far  as  I  know  have  not  been  satisfactorily  explained.  Why,  for 
instance,  should  there  be  so  marked  a  discrepancy  in  the  fre- 
quency with  which  the  ulnar  and  radial  are  affected  ? 

This  matter  will  again  be  referred  to  in  considering  the  eti- 
ology. 

It  should  also  be  mentioned  that  arteriosclerosis  of  the  nodular 
variety  is  encountered  in  some  arteries  with  greater  frequency 
than  in  others.  These  are  such  as  do  not  run  in  straight  or 
nearly  straight  directions,  but  make  numerous  turns  in  their 
course  or  give  off  branches  at  a  shar|)  angle.  The  sclerotic  ])rocess 
is  here  found  at  the  points  wliciice  the  branches  dejjart  or  where 
the  vessel  undergoes  a  bend  or  curve.     A  glance  at  Bregmann's 


ARTERIOSCLEROSIS  741 

tables,  quoted  by  Romberg,  and  compiled  with  special  reference  to 
the  nodular  form,  shows  that  the  abdominal  aorta  heads  the  list, 
while  the  common  carotid,  internal  carotid,  ascending  aorta,  and 
cerebral  arteries  follow  close  after  in  this  order. 

On  the  other  hand,  the  radial  is  generally  affected  with  the 
diffuse  form,  owing  probably  to  its  nearly  direct  course  and  the 
arrangement  of  its  not  numerous  branches,  conditions  which  per- 
mit uniformly  high  blood-pressure,  and  hence  development  of 
sclerosis  throughout  its  length. 

Associated  with  sclerotic  changes  in  the  vascular  system  are 
alterations  of  a  similar  nature  in  the  various  organs,  particularly 
heart,  kidneys,  and  liver.  In  the  senile  form  the  heart  may  be 
decreased  in  size,  whereas  in  the  diffuse  variety,  that  encountered 
in  comparatively  young  and  robust  men,  the  heart  sometimes 
reaches  enormous  dimensions.  Councilman  found  instances  in 
which  the  heart  weighed  two  and  nearly  three  times  the  normal. 
The  myocardium  is  apt  to  show  fibrous  degeneration,  the  coro- 
naries  to  be  sclerotic,  and  the  aortic  valve  to  be  opaque,  sclerotic, 
and  in  some  cases  incompetent. 

The  kidneys  are  especially  likely  to  show  the  sclerotic  change 
on  microscopic  examination,  although  to  the  naked  eye  the  changes 
may  be  so  slight  as  to  be  easily  overlooked.  The  capsule  is  adher- 
ent and  somewhat  roughened  on  its  surface,  which  may  present 
dark  red  depressed  areas  due  to  atrophy.  The  capillaries  of  the 
glomeruli  are  thickened  and  may  be  obliterated  and  exhibit  ex- 
tensive hyaline  degeneration.  Atrophic  changes  may  be  present 
in  the  liver,  particularly  in  connection  with  senile  arteriosclerosis. 

Etiology. — The  great  frequency  of  sclerotic  changes  in  the 
arteries  of  old  people  very  naturally  attracted  attention  and  sug- 
gested a  close  etiological  connection  between  age  and  this  disease. 
It  has  been  thought  directly  due  to  senility,  and  hence  a  necessary 
part  of  advanced  years.  That  arteriosclerosis  is  not  an  invariable 
accompaniment  of  age,  however,  is  well  known,  and  Gibson  states 
that  when  Thomas  Parr  died  at  the  age  of  one  hundred  and  fifty- 
two  his  arteries  were  found  by  Harvey  to  be  free  from  any  evi- 
dence of  degeneration.  Such  facts  indicate  that  to  the  mere  influ- 
ence of  age  per  se  cannot  be  attributed  the  development  of  arterial 
degeneration.  The  explanation  given  by  Romberg  of  the  connec- 
tion between  the  two  conditions  seems  to  me  to  be  the  best  I  have 


742  DISEASES  OF  THE  HEART 

yet  seen,  and  is,  that  when  arteriosclerosis  is  found  in  an  old  man, 
it  is  because  the  conditions  of  blood-pressure  which  lead  to  the 
change  have  been  operative  during  his  many  years,  and  therefore 
have  come  to  manifest  themselves  more  extensively  than  in  a 
younger  individual. 

Males  are  without  doubt  more  often  and  extensively  affected 
with  this  change  than  are  females.  This  is  owing  not  to  any 
special  influence  inherent  in  sex,  but  to  the  greater  exposure  of 
men  to  occupations,  habits,  and  conditions  of  life  in  general  which 
affect  blood-pressure  injuriously.  The  influence  of  occupations 
which  necessitate  arduous  physical  exertion,  and  thereby  subject 
the  arterial  system  to  strain,  has  long  been  recognised  and  empha- 
sized, particularly  by  the  English,  Thus  day  labourers,  smiths, 
miners,  etc.,  are  very  apt  to  develop  arteriosclerosis,  sometimes  at 
a  comparatively  early  age,  and  Romberg  points  out  that  in  them 
it  is  the  vessels  of  the  extremities  that  are  specially  prone  to  dis- 
ease. It  is  probable,  also,  that  among  the  labouring  classes  other 
factors  are  at  work  beside  physical  toil,  such  as  abuse  of  alcohol 
and  syphilis,  l^evertheless,  strain  of  the  vascular  coats  by  severe 
and  oft-repeated  muscular  effort  cannot  be  ignored  in  the  produc- 
tion of  sclerosis. 

Of  diseases  which  lead  to  this  degenerative  process  syphilis 
is  perhaps  the  most  important.  Its  relation  to  the  form  of  endar- 
teritis known  as  obliterans  was  described  by  Heubner,  and  is  quite 
generally  recognised.  Chronic  lead  poisoning  and  chronic  alco- 
holism are  also  recognised  etiological  factors,  as  is  likewise  gout. 
How  these  act  is  not  quite  clear,  whether  as  suggested  by  Traube 
by  causing  persistent  augmentation  of  blood-pressure  or  through 
the  action  of  their  poisons  directly  on  the  vascular  coats.  The 
excessive  use  of  tobacco  is  also  believed  by  some  w^riters  (Iluchard, 
Romberg)  to  cause  arteriosclerosis,  particularly  of  the  coronary 
arteries.  Romberg  likewise  states  that  neurasthenic  subjects  are 
prone  to  arterial  degeneration,  as  he  believes,  in  consequence  of 
the  frequent  alternations  in  blood-pressure  occasioned  by  their 
unstable  and  excitable  nervous  state. 

The  manner  in  which  these,  and  other  predisposing  conditions 
to  be  mentioned  presently,  act  in  the  production  of  arterial  degen- 
erations has  long  been  thought  to  be  through  the  persistent  in- 
crease of  blood-pressure  occasioned  by  them.     Nevertheless  expla- 


ARTERIOSCLEROSIS  743 

nation  based  on  such  hypothesis  was  not  altogether  satisfactory 
and  did  not  clearly  account  for  the  pathology  or  etiology  of  the 
changes  observed.  In  the  light  of  Thoma's  investigations  and 
views,  however,  we  are  now  able  to  understand  much  in  the  etiol- 
ogy which  was  before  obscure. 

It  will  be  remembered  that,  according  to  his  view,  the  thicken- 
ing of  the  intima  is  an  attempt  at  the  preservation  of  the  normal 
relation  existing  between  the  calibre  of  the  vessel  and  the  pressure 
of  its  contained  blood.  The  loss  of  such  proper  relation  or  equi- 
librium, as  it  may  be  termed,  is  brought  about  either  by  dilata- 
tion of  the  artery  in  consequence  of  lessened  elasticity  or  by  dimi- 
nution in  the  volume  of  the  contents.  Loss  of  elastic  resistance 
on  the  part  of  the  vessel  is  due  to  degeneration  and  atrophy  of  the 
elastic  fibres  of  the  media,  and  this  destructive  change  in  the  mid- 
dle coat  may  be  due  to  the  long  continuance  of  excessive  blood- 
pressure  or  to  sudden,  frequent  alternations  of  blood-pressure. 

Diminution  of  the  volume  of  blood  is  seen  very  much  less  fre- 
quently, but  is  met  with  in  the  arteries  of  amputated  extremities 
(Komberg),  and,  according  to  the  same  author,  in  the  renal  artery 
in  interstitial  nephritis.  Of  course  the  former  requirement — i.  e., 
increased  pressure — is  far  more  often  and  widely  operative  than 
is  lessened  blood-pressure.  Accordingly,  when  we  have  to  do 
clinically  with  arteriosclerosis  we  have  to  seek  out  some  under- 
lying condition,  disease,  occupation,  or  habit,  that  has  caused 
long-continued  and  greater  internal  or  endarterial  strain  than  the 
vessel  was  able  to  bear.  Slowly  the  middle  coat  has  been  forced  to 
give  way  before  the  intravascular  blood-pressure,  pari  passu  the 
intima  has  taken  on  compensatory  thickening  and  by  degrees  the 
sclerotic  process  has  declared  itself. 

In  some  individuals  blood-pressure  has  been  abnormally  high 
quite  uniformly  throughout  the  body  and  arteriosclerosis  is  gen- 
eral. More  commonly,  perhaps,  the  conditions  influencing  the 
change  are  local  and  the  degeneration  is  confined  to  or  at  least 
far  more  pronounced  in  certain  parts,  as  extremities,  brain,  coro- 
naries,  etc.  For  example,  the  frequency  with  which  the  anterior 
tibial  is  involved  is  explained  by  the  fact  that  this  artery  is  com- 
pelled to  bear  the  distending  weight  of  a  column  of  blood  which  is 
heavy  by  reason  of  hydrostatic  pressure  (Romberg). 

It  has  been  frequently  and  forcibly  pointed  out   (Fraenkel, 


744  DISEASES  OP  THE  HEART 

Hasenfeld)  that  corpulent  persons  of  a  sedentary  mode  of  life  are 
especially  prone  to  the  development  of  sclerosis  in  the  splenic, 
hepatic,  and  superior  mesenteric  arteries,  and,  according  to  Hasen- 
feld, earlier  in  these  than  elsewhere. 

The  explanation  is,  that  owing  to  their  sedentary  pursuits  and 
their  habitual  consumption  of  more  food  than  the  requirements  of 
their  inactive  lives  demand  (luxus  consumption)  the  vessels  of 
their  digestive  organs  are  persistently  overtaxed.  In  other  words, 
blood-pressure  within  them  is  habitually  too  high.  In  time  abnor- 
mally high  and  sustained  pulse-tension  is  everywhere  established, 
more  or  less  wide-spread  arteriosclerosis  develops,  and  in  conse- 
quence secondary  cardiac  hypertrophy  (Fraentzel.'s  idiopathic  en- 
largement of  the  heart)  results. 

Another  interesting  phase  of  this  question  of  blood-pressure 
relates  to  the  development  of  sclerosis  in  vessels  which  are  ex- 
posed to  varying  degrees  of  pressure,  oscillations  from  low  to 
high  pressure,  "  schwanlvungen  "  (Romberg).  Such  alternations 
subject  the  artery  to  undue  strain  and  probably  account  for  the 
sclerotic  change  so  frequently  present  in  the  arteries  of  the  arms 
of  workingmen.  According  to  Romberg,  they  also  explain  the 
fact  that  sufferers  from  migraine  sometimes  manifest  sclerosis  of 
the  arteries  of  the  side  of  the  head  affected  by  the  pain. 

It  is  on  this  hypothesis  likewise  that  we  may  explain  the  pre- 
ponderance of  arteriosclerosis  in  the  cerebral  vessels  of  persons  who 
are  engaged  in  literary  pursuits  or  whose  occupations  call  for  spe- 
cial activity  on  the  part  of  the  brain  during  a  certain  number  of 
hours  each  day.  May  it  not  be  for  this  reason  that  many  an 
ambitious  business  man  succumbs  to  the  stress  of  modern  com- 
mercial life  ?  Romberg  explains  the  greater  frequency  of  coro- 
nary sclerosis  in  hypertrophied  hearts  as  compared  with  those  that 
are  not  hypertrophied,  on  the  ground  that  coronary  blood-pres- 
sure is  higher  in  the  former  on  account  of  their  more  forcible 
contractions. 

If  his  view  is  correct,  then  one  is  tempted  to  query  if  the  car- 
diac excitement  experienced  by  stock-brokers  and  men  of  affairs 
under  the  influence  of  rapid  fluctuations  of  the  stock  or  grain 
market  may  not  have  much  to  do  with  the  relatively  great  fre- 
quency of  coronary  angina  in  modern  business  men.  In  illustra- 
tion of  the  important  etiological  influence  exerted  by  variations 


ARfERIOSCLEROSIS  745 

of  blood-pressure  in  circumscribed  areas,  Romberg  cites  the  re- 
markable case  reported  by  Erb  of  an  ardent  angler  who  developed 
a  high  degree  of  arteriosclerosis  in  the  lower  extremities,  in  con- 
sequence, it  is  thought,  of  his  standing  and  walking  for  hours 
together  in  the  cold  water  of  the  streams  where  he  fished. 

Additional  instances  of  the  injurious  effect  of  long-continued 
high  blood-pressure  are  seen  in  the  degenerative  changes  found  in 
the  pulmonary  artery  of  mitral  patients  and  in  chronic  phthisis 
as  well  as  the  general  arteriosclerosis  of  diabetic  patients  (Rom- 
berg). In  short,  upon  the  basis  of  Thoma's  conclusions  we  are  now 
able  to  understand  many  a  case  of  arteriosclerosis  the  development 
of  which  was  previously  almost  unintelligible. 

Symptoms. — Arteriosclerosis  is  latent  so  long  as  it  is  of 
minor  degree  and  not  very  wide-spread.  When  at  length  symptoms 
are  produced,  they  depend  upon  the  degree  and  distribution  of  the 
process  and  the  organs  affected.  In  some  cases  the  clinical  picture 
is  that  of  renal  inadequacy,  in  others  of  cardio-vascular  disorder, 
in  others  again  of  disturbed  cerebral  circulation,  and  in  still  others 
of  interference  with  the  blood-supply  to  the  extremities,  digestive 
organs,  or  heart-muscle,  as  the  case  may  be. 

Sclerosis  of  the  renal  arteries  may  be  secondary  to  already  ex- 
isting interstitial  nephritis  in  consequence  of  diminished  supply 
of  blood  to  the  renal  capillaries,  but  in  most  cases  it  precedes  or 
accompanies  the  development  of  the  nephritis.  The  augmented 
blood-pressure  occasioned,  first  declares  itself  clinically  by  in- 
creased secretion  of  urine,  particularly  at  night.  Examination  of 
the  urine  in  this  early  stage  generally  shows  nothing  more  than 
a  lowered  specific  gravity.  When  at  length  the  sclerosis  has  be- 
come so  extreme  as  to  materially  interfere  with  flow  of  blood  in 
the  renal  capillaries,  the  urine  grows  scanty,  and  is  apt  to  present 
characters  like  those  of  genuine  contracting  kidney. 

In  these  cases  there  is  apt  to  be  more  or  less  sclerosis  of  the 
arteries  of  other  parts,  particularly  the  heart,  or  general  pulse  ten- 
sion becomes  too  high  to  be  successfully  combated  by  the  hyper- 
trophied  left  ventricle,  and  symptoms  of  cardiac  incompetence  are 
added  to  those  of  renal  disease.  Thus  I  recall  the  case  of  a  middle- 
aged  physician  who,  aside  from  cardiac  breathlessness,  developed 
symptoms  of  serious  renal  inadequacy.  Urine  grew  persistently 
scanty,  contained  an  occasional  trace  of  albumin,  but  rarely  casts. 


746  DISEASES  OF  THE  HEART 

He  ultimately  died  with  symptoms  that  were  urromic  rather  than 
cardiac,  and  the  autopsy  disclosed  almost  complete  obliteration  of 
the  renal  arteries. 

In  other  cases  the  picture  is  that  of  slowly  increasing,  or  per- 
haps suddenly  induced,  failure  of  heart-power,  with  renal  symp- 
toms of  very  inferior  importance.  Only  to-day  I  examined  a  man 
of  seventy-one  who  for  two  years  past  has  noticed  breathlessness, 
which  of  late  has  become  serious  cardiac  dyspnoea.  For  more  than 
twenty  years  he  has  had  increased  nocturnal  micturition,  but  no 
other  evidence  of  renal  disease.  He  has  been  closely  confined  to 
his  desk  daily,  and  has  been  "  a  pretty  heavy  eater,  particularly 
at  breakfast."  His  chest  is  capacious  and  abdorainal  corpulence 
is  quite  marked.  The  radials,  temporals,  and  carotids  are  stiff, 
and  the  heart  is  enormously  enlarged,  its  impulse  feeble,  and  its 
sounds  distant  and  muffled.  This  case  is  a  fair  illustration  of  the 
etiology  and  symptomatology  of  the  cases  in  which  the  clinical  pic- 
ture is  what  may  be  termed  cardio-vascular,  the  chief,  it  may  be  the 
only,  complaint  being  dyspna?a  of  effort. 

Many  such  cases,  like  the  foregoing,  very  well  represent  the 
clinical  picture  of  chronic  myocarditis.  In  others,  sj'mptoms  of 
failing  heart-power  and  of  chronic  interstitial  nephritis  are  so  in- 
timately blended  as  to  make  it  difficult  to  determine  definitely 
which  organ  is  the  more  seriously  involved.  In  others  again,  gly- 
cosuria and  renal  cirrhosis  precede  the  symptoms  of  vascular  and 
cardiac  disease,  yet  when  the  latter  become  marked  they  may  domi- 
nate the  scene.  In  all  these  eases,  when  cardiac  incompetence  su- 
pervenes, it  is  apt  to  prove  most  serious  and  to  progress  under  the 
every-day  appearance  of  increasing  and  unconquerable  stasis, 
since  the  extreme  degree  of  peripheral  resistance  incident  to  arte- 
rial rigidity  renders  restoration  of  heart-power  impossible.  They 
have  been  sufficiently  portrayed  in  preceding  pages  and  do  not  re- 
quire repetition. 

In  comparatively  few  cases  the  symptoms  are  mainly,  almost 
exclusively,  referable  to  the  arteriosclerosis  as  such.  The  arteries 
everywhere  feel  wiry  and  nodular,  like  a  string  of  beads,  or  thick- 
ened and  tortuous,  and  the  pulse  is  small  and  weak.  The  super- 
ficial veins  stand  out  prominently;  the  heart  manifests  slight  if 
any  change,  being  in  some  moderately  and  in  others  not  at  all 
enlarged ;  the  urine  is  scanty  and  of  poor  quality,  and  if  any  albu- 


ARTERIOSCLEROSIS  747 

mill  is  present,  it  is  a  mere  trace,  while  casts  are  scanty,  being  hya- 
line or  granular;  the  patient  complains  of  increasing  inability 
to  work  or  exercise;  appetite  and  digestion  fail;  slight  oedema 
appears  at  the  ankles ;  the  individual  emaciates,  grows  sallow, 
pale,  steadily  more  feeble,  and  at  length  takes  to  bed  and  dies  from 
what  appears  to  be  general  asthenia. 

I  have  notes  of  such  a  typical  case  in  an  Englishman  who  was  a 
farmer  of  about  sixty-eight  years  of  age.  Up  to  a  year  or  so  prior 
to  my  seeing  him  he  was  hale  and  hearty,  and  able  to  perform 
active  work  of  a  not  too  severe  kind. 

Examination  disclosed  no  distinct  evidence  of  heart  or  renal 
disease,  but  the  radials,  ulnars,  temporals,  femorals,  and  tibials 
all  felt  hard  and  empty  and  most  of  them  contained  deposits  of 
lime  that  gave  them  a  pronounced  beady  character.  Venous  stasis 
was  evident  in  the  turgescent  veins,  palpable  liver,  and  slight  pit- 
ting of  the  ankles  and  shins.  He  did  not  complain  especially  of 
dyspnoea,  but  was  much  concerned  over  his  growing  weakness  and 
loss  of  weight. 

Treatment  benefited  him  for  a  time,  but  he  ultimately  grew  too 
feeble  to  report  at  my  office,  and  as  he  resided  in  the  country  was 
lost  sight  of.  It  was  ultimately  learned,  however,  that  he  died 
after  a  few  months  of  what  appeared  to  be  general  feebleness  with 
failing  circulation.  In  his  case,  as  in  many,  the  heart  seemed  to 
be  comparatively  unaifected  and  the  difficulty  of  circulation  to  be 
due  to  the  impermeability,  so  to  speak^  of  the  arteries. 

The  rigidity  of  the  arterial  system  interferes  with  proper  dis- 
charge into  the  capillaries — neither  are  the  arteries  able  to  receive 
the  full  supply  of  blood  sent  from  the  veins,  and  stasis  occurs. 

In  a  considerable  proportion  of  cases  the  clinical  manifesta- 
tions are  not  those  of  disturbed  circulation  in  general,  but  of  dimin- 
ished or  abolished  blood-supply  to  a  part,  as  the  brain,  extremities, 
heart,  etc.  The  result  is  perverted  function  and  structural  altera- 
tion of  a  more  or  less  serious  kind.  In  some  instances  such  disturb- 
ances are  plainly  apparent,  while  in  others  the  manifestations  of 
arterial  degeneration  are  obscure  and  often  misinterpreted  or  over- 
looked altogether. 

Thus  sclerosis  of  the  cerebral  arteries  may  be  shown  by  impair- 
ment of  memory  and  intellection,  headache,  transient  vertigo,  espe- 
cially upon  quickly  assuming  the  erect  position,  change  in  disposi- 


748  DISEASES  OP  THE  HEART 

tion,  increasing  weakness,  in  a  word,  by  tlie  manifold  symptoms 
due  to  cerebral  ana?mia  or  areas  of  softening  (enceplialomalacia) 
which  result  from  the  shutting  off  of  blood-supply  to  definite  areas. 
One  should  not  forget  also  that  when  epilepsy  develops  at  or  after 
middle  age,  it  may  be  due  to  arteriosclerosis  within  the  brain 
(Hochhaus).  Disease  of  these  vessels  is  also  a  very  frequent,  ac- 
cording to  Romberg  the  most  frequent,  cause  of  apoplexy.  There 
may  be  either  luinnorrhage  into  the  brain  from  rupture  of  a  miliary 
aneurysm,  a  condition  of  the  arteries  shown  by  Charcot  to  be  very 
common,  or  the  apoplectic  seizure  may  result  from  thrombosis  of 
a  narrowed  cerebral  artery. 

Sclerosis  of  the  arteries  in  the  medulla  is  a  recognised  cause 
of  slowness  of  the  pulse  and  of  recurrent  bradycardia  known  as 
Stokes-Adams  disease,  and  which  has  been  previously  considered. 
(See  page  627.) 

Sclerosis  of  the  arteries  of  the  feet  and  legs  is  not  uncommon, 
but  apart  from  the  change  it  creates  in  the  elasticity  of  the  vessel — 
i.  e.,  stiffness  and  tortuosity,  as  perceived  by  the  palpating  finger — ■ 
it  does  not  often  lead  to  serious  disturbance  of  circulation  in  the 
region  supplied  by  the  sclerotic  artery.  The  sclerosis  may,  how- 
ever, according  to  Erb,  be  responsible  for  disorders  of  sensation 
and  motion,  vaso-motor  and  even  trophic 'disorders.  The  first  may 
be  shown  by  paraesthesia,  formication,  pain,  and  a  feeling  of  heat 
or  coldness;  disorders  of  motility,  by  intermittent  lameness  and 
extreme  degrees  of  arterial  narrowing  by  cramps,  rigidity,  etc. ; 
vaso-motor  disturbances,  by  coldness,  pallor,  cyanosis;  and  nutri- 
tional disorders,  by  circumscribed  sloughing  of  the  skin.  In  cases 
of  obliteration  from  sclerosis,  as  is  well  known,  there  may  be  local- 
ized gangrene  (senile  gangrene). 

According  to  Romberg,  sensory  and  motor  disturbances  make 
their  appearance  at  first  only  when  the  muscles  are  put  in  use — i.  e., 
when  tlicre  is  a  call  for  more  blood  to  the  part  than  can  be  fur- 
nished by  the  thickened  arteries.  In  more  advanced  degenerations 
these  disturbances  are  produced  by  insignificant  movements,  and 
at  length  the  limb  becomes  stiff  and  useless. 

Not  only  are  vaso-motor  neuroses,  such  as  pain,  redness,  swell- 
ing, stiffness,  etc.,  phenomena  of  arteriosclerosis,  but,  according  to 
Romberg,  there  may  appear  symptoms  of  Reynaud's  disease,  cyano- 
sis, pallor,  and  even  gangrene  of  portions  of  the  skin,  such  phenom' 


ARTERIOSCLEROSIS  749 

ena  being  particularly  liable  to  affect  the  fingers.  Fortunately, 
however,  such  serious  disturbances  are  rare,  and  for  the  most  part 
only  minor  degrees  of  sensory  and  vaso-motor  perversions  are 
present. 

The  heart  may  be  affected  by  arteriosclerosis  in  either  or  both 
of  two  ways :  It  may  be  degenerated  and  feeble  in  consequence  of 
thickening,  narrowing  or  thrombosis  of  the  coronaries,  with  angina 
pectoris  and  the  symptom-complex  of  myocardial  incompetence,  or 
the  heart  may  be  secondarily  hypertrophied  in  consequence  of 
diffuse  sclerosis  of  the  arteries  supplying  the  abdominal  viscera. 
Hasenfeld  has  dwelt  on  the  intimate  connection  between  sclerosis 
of  the  mesenteric  vessels  and  general  cardiac  hypertrophy,  and 
Romberg  also  states  that  it  is  degeneration  of  these  arteries  which 
calls  forth  secondary  hypertrophy  of  the  left  ventricle.  Extensive 
vascular  change  of  the  brain  and  extremities  may  exist,  he  states, 
without  appreciable  enlargement  of  the  heart.  This  coincides 
with  my  clinical  experience,  for  the  largest  and  most  inadequate 
hearts  I  have  ever  seen  have  been  in  men  whose  abdominal  cor- 
pulence and  sedentary  lives  have  furnished  the  conditions  neces- 
sary for  the  development  of  vascular  disease  in  the  splanchnic  area. 
Moreover,  their  stiffened  radials  and  high-tension  pulse  have  borne 
out  the  correctness  of  that  assumption.  On  the  other  hand,  I  have 
seen  old  men  with  emaciated  abdomens,  peripheral  arteries  that 
were  like  wires  strung  with  tiny  beads,  and  feeble,  even  flickering 
pulses,  and  yet  whose  hearts  could  not  be  made  out  as  hyper- 
trophied. In  some  of  these  cases,  to  be  sure,  pulmonary  emphy- 
sema renders  the  results  of  percussion  uncertain,  but  the  clinical 
picture  is  that  of  adynamia  or  of  a  cachexia,  but  not  of  myocardial 
failure,  as  in  men  of  the  other  type. 

Lastly,  there  is  still  another  group  of  cases  which  present  them- 
selves in  guise  of  chronic  bronchitis  and  emphysema.  They  are 
usually  at  or  past  middle  age,  not  confined  to  either  sex,  yet  in  my 
experience  more  often  males  of  the  labouring  class.  The  vascular 
system  is  everywhere  stiff,  urine  is  of  poor  quality  or  may  contain 
a  small  amount  of  albumin,  and  there  is  manifest  hypertrophy  of 
the  right  ventricle.  This  may  be  due  in  part  to  the  emphysema, 
but  a  contributing  factor  of  importance  is  the  sclerosis  of  the  pul- 
monary arteries.  It  is  not  always  easy  to  determine  whether  this 
disease  of  the  pulmonary  vessels  is  primary  or  secondary,  but  as  it 


750  DISEASES  OP  THE   HEART 

is  associated  with  retrograde  change  of  tlie  aortic  system  it  is  fair 
to  assume  that  it  plajs  a  role  in  the  causation  of  the  emphysema 
and  bronchial  catarrh. 

For  the  most  part  the  course  of  this  vascular  disease  is  slow 
and  iijdefinite.  Years  are  usually  consumed  in  its  development, 
and  even  after  symptoms  appear  the  course  is  protracted  or  more 
or  less  rapid,  according  to  the  portion  of  the  arterial  system  chiefly 
affected  and  to  the  degree  of  the  sclerotic  change. 

Physical  Signs. — Inspection. — There  are  two  main  types  of 
individuals  with  arteriosclerosis.  In  one  class  they  are  large  and 
imposing,  more  or  less  corpulent  and  with  rather  too  flabby  abdom- 
inal walls.  In  such,  there  may  or  may  not  be  evidence  of  vascular 
disease  in  the  peripheral  arteries.  The  other  type  is  quite  the  re- 
verse. The  individual  is  thin,  looks  ill-nourished,  and  the  tem- 
poral, perhaps  also  the  carotid,  arteries  are  seen  distinctly,  the 
former  looking  like  stiff  tortuous  cords  and  pulsating  visibly. 
Superficial  veins  are  also  prominent,  but  cyanosis  is  not  present. 
The  only  other  information  obtained  by  inspection  relates  to 
changes  in  the  strength  and  location  of  the  apex-beat,  and  to  epi- 
gastric pulsation,  signs  which  may  be  directly  connected  with 
arteriosclerosis,  yet  may  be  independent  of  the  same. 

Palpation. — This  is  the  best  and  usually  most  reliable  means 
of  detecting  arterial  degeneration.  If  an  artery  which  rests  on  a 
firm  foundation,  as  the  radial  or  tibial,  is  carefully  palpated,  it  is 
perceived  to  be  thicker  and  stiffer  than  nornuil.  It  can  be  rolled 
beneath  the  finger  like  a  cord,  and  the  vessel  is  difficult  to  compress. 
In  many  cases  this  is  all,  but  in  others  the  vessel  is  tortuous,  and 
when  the  finger  is  passed  along  its  course,  presents  small  elevations 
that  feel  hard  like  beads,  and  hence  lead  us  to  speak  of  the  vessel 
as  beady.  In  some  instances  the  artery  shows  minute  elevations, 
which  when  carefully  studied  are  found  to  be  dilatations  of  the 
vascular  wall — in  other  words,  miliary  aneurysms. 

Particular  attention  should  be  paid  to  the  cervical  arteries, 
noting  their  position,  size,  regularity  or  smoothness,  rigidity,  etc., 
since  changes  in  tlicin  may  furnish  valuable  hints  concerning  the 
state  of  the  aorta  and  inferentially  of  the  coronaries.  When  the 
arch  of  the  aorta  is  tliin-walled  and  dilated  it  may  sometimes  be  felt 
pulsating  abnormally  high  up  in  the  sui)rasternal  fossa.  Litten  is 
authority  for  the  statement  that  when  the  abdominal  aorta  is  scle- 


ARTERIOSCLEROSIS  751 

rotic  and  accessible  to  palpaticjii,  thrill  is  elicited  by  very  much  less 
pressure  than  is  required  if  the  vessel  is  healthy. 

Percussion  is  of  value  only  in  the  detection  of  changes  in  the 
size  of  the  heart  secondary  to  vascular  disease.  It  may,  therefore, 
by  demonstrating  hypertrophy  of  the  left  ventricle,  afford  a  certain 
amount  of  corroborative  information.  Careful  and  deep  percus- 
sion of  the  areas  overlying  the  ascending  portion  of  the  aortic  arch 
may  detect  a  slight  degree  of  dulness  due  to  dilatation  of  the  vessel. 
In  such  a  case  resonance  is  apt  to  be  impaired  in  the  first  and  sec- 
ond right  interspaces  close  to  the  sternum.  Dilatation  and  elonga- 
tion of  the  arch  may  displace  the  heart  downward,  the  same  as  does 
true  aneurysm ;  and  hence  in  cases  in  which  the  aorta  is  suspected 
of  being  sclerotic,  it  is  well  to  percuss  the  heart  carefully,  with 
view,  if  possible,  to  ascertaining  its  exact  location. 

Auscultation. — Almost  the  only  value  of  this  means  of  investi- 
gation lies  in  the  study  of  the  second  sound  in  the  aortic  area.  This 
tone  is  normally  more  intense  than  is  the  pulmonic  second  in  per- 
sons after  thirty  years  of  age,  and  hence  it  is  the  quality  of  this 
sound  more  than  its  mere  intensification  that  is  significant.  Gen- 
eral arteriosclerosis  causes  accentuation  of  the  aortic  second  tone, 
but  so  also  do  other  conditions,  especially  chronic  interstitial  neph- 
ritis. Taken  in  connection  with  left-ventricle  hypertrophy,  un- 
due intensification  of  this  sound  is  significant  of  arterial  or  renal 
disease  or  botb.  If  the  sound  is  not  only  intensified  but  is  also 
sharply  ringing,  even  of  a  metallic  quality  and  is  associated 
with  stiff  arteries  in  persons  of  middle  age,  it  is  generally  consid- 
ered to  indicate  sclerosis  of  the  aorta.  Should  the  sound  be  not 
quite  pure,  as  well  as  accented,  it  is  likely  that  the  valve  is  also 
involved  in  the  degenerative  process,  l^ot  infrequently  in  persons 
whose  vessels  are  resisting,  there  is  a  systolic  murmur  heard  along 
the  course  of  the  ascending  arch,  and  when  present  is,  in  the 
absence  of  signs  and  symptoms  of  aneurysm,  to  be  regarded  as 
due  to  roughening  or  dilatation  or  both  of  the  aorta,  not  of  steno- 
sis of  the  ostium.  Any  other  modifications  of  the  cardiac  sounds 
are  indicative  of  secondary  or  associated  changes  in  the  heart- 
muscle  and  valves. 

Diagnosis. — The  recognition  of  sclerotic  changes  in  periph- 
eral vessels  that  can  be  reached  by  the  palpating  finger,  as  radial, 
ulnar,  tibial,  etc.,  is  a  very  simple  matter,  and  has  been  sufficiently 


752  DISEASES   OF   THE  HEART 

described  under  palpation.  It  is  far  otherwise,  however,  with  the 
diagnosis  of  sclerosis  of  the  arteries  within  the  cranial  and  other 
cavities.  In  such,  diagnosis  is  usually  a  matter  of  inference  in- 
stead of  absolute  demonstration,  and  must  be  arrived  at  by  study 
of  the  patient's  history,  age,  symptoms,  etc.  It  is  manifestly 
beyond  the  scope  of  this  work  to  discuss  the  diagnosis  of  disease 
of  the  cerebral  vessels.  It  may  be  stated,  however,  that  tortuosity 
and  rigidity  of  the  temporals  may,  in  connection  with  the  head 
symptoms  previously  noted,  be  taken  to  point  strongly  to  sclerosis 
of  the  cerebral  arteries.  If  doubt  still  remains,  or  the  external 
vessels  are  negative,  the  ophthalmoscope  may  be  appealed  to  and 
is  said  to  furnish  early  and  reliable  information  concerning  the 
state  of  the  cerebral  arteries  (Thoma,  Eehlmann,  Koenig).  The 
changes  said  to  indicate  sclerosis  are  pulsation  and  tortuosity  of  the 
retinal  artery  (when  not  due  to  chlorosis  or  anaemia),  opacity  of 
its  coats,  narrowing,  and  it  may  be  thrombosis  of  the  artery  of  the 
papilla,  and  miliary  aneurysms  and  punctate  haemorrhages  into  the 
retina,  the  choroid,  and  the  enveloping  capsule  of  the  optic  nerve 
(Koenig). 

The  diagnosis  of  sclerosis  of  the  aorta  cannot  always  be  defi- 
nitely made.  Romberg  states  that  the  condition  of  peripheral 
vessels,  as  radials,  affords  no  criterion  of  that  of  the  aorta,  and 
hence  stiffness  of  the  arm  or  leg  arteries  does  not  warrant  a  con- 
clusion that  the  aorta  is  also  sclerotic.  The  state  of  the  latter 
must  be  inferred,  therefore,  from  careful  study  of  the  cervical  ves- 
sels and  of  changes  in  the  size  of  the  heart  or  of  its  sounds.  If 
the  carotids  appear  healthy,  if  the  heart  is  not  appreciably  en- 
larged nor  displaced,  and  the  aortic  second  tone  is  not  unduly  ac- 
centuated, then  the  aorta  is  probably  healthy.  If,  on  the  contrary, 
the  carotids  are  unyielding,  the  subclavians  are  situated  abnor- 
mally high  and  feel  stiff,  if  the  left  ventricle  is  hypertrophied,  and 
lastly,  but  not  least,  if  the  aortic  second  sound  is  ringing  and  metal- 
lic, there  is  probably  sclerosis  of  the  ascending  portion  of  the  arch. 

The  question  of  the  existence  or  not  of  arteriosclerosis  within 
the  domain  of  the  splanchnic  nerves  may  present  great  difficulties. 
The  recognition  of  stiffened  radials  in  a  corpulent  individual  who 
complains  of  dyspnoea  of  effort  out  of  proportion  to  recognisable 
changes  in  the  heart,  renders  extremely  probable  a  similar  state  of 
the  vessels  deeply  situated  in  the  abdominal  cavity.    If,  on  the  eon- 


ARTERIOSCLEROSIS  T53 

trary,  accessible  arteries  are  not  stiff;,  one  must  depend  for  diagno- 
sis on  the  history,  symptoms,  degree  of  blood-pressure,  and  adequacy 
as  well  as  size  of  the  heart.  A  history  of  sedentary  pursuits 
and  of  luxus  consumption;  gradually  developed  and  increasing 
shortness  of  breath ;  abdominal  corpulence ;  high  tension  but  slow 
pulse;  cardiac  hypertrophy  without  dilatation;  these  point 
strongly  to  arteriosclerosis  as  the  cause  of  the  symptoms. 

In  suspected  cases  one  should  test  the  efficiency  of  the  heart- 
muscle  as  well  as  search  carefully  for  indications  of  overstrain  of 
the  right  ventricle.  If  the  pulse  is  unduly  rapid  and  feeble  during 
repose,  if  cardiac  dulness  is  increased  transversely  and  downward 
with  pulsation  in  the  epigastrium,  if  superficial  veins  are  engorged, 
there  is  reason  to  conclude  that  the  heart  is  no  longer  quite  ade- 
quate and  that  the  dyspnoea  is  cardiac.  Then  if  on  the  patient's 
making  extra  exertion,  as  by  hopping  about  the  room,  the  action 
of  the  heart  grows  unduly  accelerated,  perhaps  irregular  or  inter- 
mittent, and  the  sounds  become  feeble,  perhaps  accompanied  by  an 
apex-murmur,  but  little  doubt  is  to  be  entertained  of  myocardial 
insufficiency. 

Even  then  the  state  of  the  internal  vascular  system  may  be  a 
matter  of  doubt.  Prolonged  high  tension  of  the  pulse,  as  shown  by 
Gaertner's  tonometer,  and  a  ringing  metallic  quality  of  the  aortic 
second  sound  strengthen  the  assumption  that  the  heart  weakness  is 
secondary  to  arteriosclerosis.  It  is,  of  course,  presupposed  that  all 
other  etiological  data  are  wanting. 

The  differential  diagnosis  of  such  cases  from  the  cardiac  insuf- 
ficiency of  the  obese  (the  so-called  fatty  heart),  is  often  impossible, 
and,  as  a  matter  of  fact,  the  two  conditions  are  not  infrequently 
combined.  In  the  obese,  however,  there  is  a  general  distribution 
of  adipose  tissue  far  in  excess  of  what  exists  where  there  is  only 
excessive  abdominal  corpulence  with  arteriosclerosis. 

Quite  recently  I  examined  a  gentleman  of  fifty-three  com- 
plaining of  breathlessness  on  more  than  moderate  exertion.  His 
abdomen  was  very  bulging  and  flabby,  while  his  extremities  and 
chest  were  rather  thin,  his  radials  were  distinctly  stiff,  but  the 
heart  was  not  appreciably  enlarged  except  on  the  left,  and  did  not 
grow  too  rapid  or  irregular  from  the  effort  of  hopping  up  and 
down  my  office.  In  this  case  I  felt  no  hesitation  in  attributing 
his  symptoms  to  arteriosclerosis,  and  not  to  myocardial  inadequacy, 
49 


754  DISEASES  OP  THE  HEART 

particularly  as  his  habits  were  such  as  tended  inevitably  to  its  de- 
velopment. Unfortunately  all  cases  are  not  so  clear,  and  hence 
necessitate  great  reserve. 

With  regard  to  the  diagnosis  of  vascular  disease  in  other  inac- 
cessible regions,  it  may  be  stated  that  coronary  sclerosis  is  not  often 
possible  of  positive  recognition.  It  may  be  assumed  when  angina 
pectoris  develops  in  a  man  past  middle  age,  when  there  is  reason- 
able evidence  of  sclerosis  of  the  aorta  and  its  great  branches  with 
subjective  and  objective  symptoms  of  myocardial  incompetence. 

Sclerosis  of  the  pulmonary  artery  cannot  be  diagnosed  with 
any  degree  of  certainty,  but  may  be  assumed  if  a  patient  with  stiff 
arteries  is  a  sufferer  from  chronic  bronchitis  and  emphysema,  and 
in  addition  there  is  unusual  hypertrophy  of  the  right  ventricle. 

Kenal  arteriosclerosis  may  be  inferred  if  in  conjunction  with 
stiffened  peripheral  vessels  there  is  nocturnal  micturition,  the 
urine  being  of  poor  quality.  When  in  an  advanced  stage  there  is 
evidence  of  positive  renal  change,  as  shown  by  albumin  and  casts, 
it  is  practically  impossible  to  say  definitely  how  much  is  due  to 
nephritis  and  how  much  to  arteriosclerosis. 

Prognosis. — This  depends  upon  the  degree  of  the  vascular 
change  discovered  and  upon  the  extent  and  nature  of  the  visceral 
disturbance  resulting  therefrom.  The  process  is  inherently  pro- 
gressive, and  I  believe  incurable.  Symptoms  may,  however,  some- 
times be  held  in  check  by  proper  treatment. 

Cardio-vascular  symptoms  are  for  the  most  part  subject  to  the 
conditions  which  influence  prognosis  in  cases  of  myocarditis,  and 
need  not  here  be  dwelt  upon.  For  the  prognosis  of  cerebral  and 
renal  arteriosclerosis  readers  are  referred  to  works  devoted  to  dis- 
eases of  the  respective  organs.  The  prognosis  of  sclerosis  of  the 
pulmonary  vessels  is  essentially  that  of  the  cardiac  or  pulmonary 
affections  to  which  it  is  secondary,  while  when  vascular  decay  of 
the  arteries  of  the  extremities  has  once  led  to  definite  disturbance 
of  circulation  the  prognosis  is  highly  unfavourable.  Progressive 
emaciation  and  loss  of  strength  in  general  arteriosclerosis  indicate 
so  serious  an  interference  with  nutrition  that  it  may  be  regarded 
as  the  coiiimencement  of  the  end. 

Treatment. — This  is  to  be  divided  into  (1)  prophylactic, 
(2)  curative,  and  (3)  symptomatic.  The  institution  of  preventive 
measures  necessitate  (A)  the  earliest  possible  recognition  of  vas- 


ARTERIOSCLEROSIS  755 

cular  change  and  (B)  the  proper  regulation  of  habits,  diet,  exercise, 
and  excretion  with  a  view  to  lessening  undue  vascular  strain  and 
correcting  injurious  fluctuations  of  blood-pressure.  The  disas- 
trous effect  of  sedentary  pursuits  must  be  counteracted  by  appro- 
priate gymnastic  and  abdominal  exercises,  including  massage  in 
cases  of  excessive  abdominal  corpulence.  Heavy  feeding  must  be 
restricted  and  its  effects  offset  by  outdoor  exercise  and  sports,  as 
golf,  hunting,  and  fishing.  Furthermore,  the  character  of  the 
dietary  should  be  revised  so  as  to  exclude  or  reduce  the  eating  of 
meats  which  are  tissue-forming  foods  and  are  also  harmful  on 
account  of  the  extractives  they  contain. 

Theoretically,  also,  the  diet  should  not  consist  of  foods  rich 
in  lime-salts,  and  as  a  matter  of  fact  Rumpf,  of  Hamburg,  cuts 
out  such  articles  from  the  dietary  of  his  patients.  He  includes 
among  such  forbidden  articles  milk,  eggs,  cheese,  rice,  and  spinach. 
For  my  part,  I  am  of  the  opinion  that  quantity  cuts  a  far  greater 
figure  than  does  quality,  since  it  is  a  matter  of  every-day  observa- 
tion that  the  individuals  who  live  the  longest  and  are  the  most 
active  with  advancing  years  are  those  who  eat  sparingly  and  of  a 
dietary  relatively  rich  in  vegetables,  cereals,  milk,  and  fruits.  I 
regard  it  as  a  good  indication  when  a  person  past  middle  age  tends 
to  lose  weight  gradually  rather  than  to  gain.  Best  of  all,  he  should 
strive  to  hold  his  weight  about  at  a  standstill  until  well  on  in 
years. 

Exercise  in  the  open  is  a  very  important  matter,  especially  for 
the  man  who  having  been  accustomed  to  plenty  of  exercise  in  col- 
lege suddenly  finds  himself  tied  down  to  his  office  desk  many  hours 
each  day.  He  should  endeavour  in  every  way  possible  to  get  out 
for  some  sort  of  active  physical  exertion.  If  his  profession  or  busi- 
ness duties  tax  his  mental  powers  severely  and  keep  him  keyed 
up  to  the  highest  pitch  day  after  day  and  month  after  month,  then 
he  should  make  whatever  sacrifice  is  necessary  to  secure  a  yearly 
vacation,  during  which  he  can  obtain  perfect  relaxation  and  recrea- 
tion. Otherwise  sclerosis  of  cerebral  or  other  arteries  will  be  his 
fate  after  middle  age. 

If,  as  is  believed,  the  splanchnic  nerves  regulate  blood-pressure 
and  irritation  of  these  nerves  increases  blood-pressure,  particularly 
within  the  abdominal  cavity,  then,  from  a  prophylactic  standpoint, 
digestive  derangements,  including  of  course  chronic  constipation, 


756  DISEASES  OF   THE   HEART 

should  be  corrected.  This  is  desirable  from  another  point  of  view 
— namely,  that  by  improving  excretion  the  system  may  be  rid  of 
toxines  which  may  be  of  influence  in  augmenting  arterial  tension, 
and  eventually  leading  to  arteriosclerosis. 

In  a  word,  the  prevention  of  degenerative  changes  in  the  blood- 
vessels calls  for  the  removal,  or  at  least  the  minimizing,  of  all  in- 
jurious influences  which  are  believed  to  derange  blood-pressure, 
and  thereby  subject  the  vascular  system  locally  and  generally  to 
strain. 

The  curative  treatment  of  arteriosclerosis  is,  I  believe,  unprom- 
ising. The  French,  and  of  late  some  German  clinicians,  as  Vie- 
rordt,  express  faith  in  the  ability  of  iodine  to  arrest  and  even  cure 
vascular  degeneration.  The  remedy  is  administered  in  the  form 
of  iodide  of  sodium  rather  than  of  potassium  because  of  its  being 
better  tolerated.  It  is  begun  in  small  doses,  2  or  3  grains  twice  or 
thrice  a  day  at  first,  and  as  the  system  learns  to  tolerate  the  remedy 
it  is  gradually  increased  until  15  grains  three  times  a  day  are 
reached.  In  this  dose  the  iodide  is  continued  over  a  long  time — i.e., 
from  eighteen  months  to  three  years — but  with  occasional  intervals 
during  which  the  drug  is  not  taken.  Yierordt  is  said  to  omit  the 
remedy  one  week  out  of  five  and  one  month  out  of  every  five  months. 
Given  in  this  manner,  and  from  the  start  increased  so  cautiously  as 
not  to  cause  undue  irritation,  he  has  seen  very  gratifying  results. 
I  have  made  repeated  attempts  to  get  my  private  patients  to  perse- 
vere in  the  use  of  iodide  of  sodium  after  the  manner  recommended 
by  Vierordt,  but  always  without  success.  It  has  invariably  disor- 
dered appetite  and  digestion,  and  at  length  has  had  to  be  discon- 
tinued. 

This  therapeutic  agent  may  favourably  affect  the  patient's  gen- 
eral condition,  and  even  the  vascular  disease  in  cases  of  syphi- 
litic origin  (although  I  believe  the  claim  is  made  that  favourable 
results  arc  obtained  even  when  there  is  no  specific  taint),  but  it  is 
very  difficult  to  see  how  any  drug  can  promote  resolution  of  the 
sclerotic  process,  or  why  it  should  be  well  to  do  so.  If  the  develop- 
ment of  connective  tissue  in  the  intima  is,  as  Thoma  believes,  a 
compensatory  process  by  which  is  attempted  to  make  good  atrophic 
changes  in  the  media,  then  how  can  any  line  of  therapy  be  bene- 
ficial that  does  not  restore  the  media  to  its  former  normal  state? 
The  iodide  may  in  some  way  prevent  or  remove  deposits  of  lime 


ARTERIOSCLEROSIS  757 

and  the  hyaline  degeneration  that  ultimately  occur  in  the  newly 
formed  connective  tissue,  but  can  it  do  more  or  would  it  be  well  to 
have  it  do  more  ? 

It  seems  to  me,  therefore,  that  when  arteriosclerosis  has  once 
become  pronounced,  our  efforts  must  be  limited  to  the  prevention 
or  lessening  of  symptoms — in  short,  must  be  symptomatic.  To  do 
this  we  must  endeavour  to  promote  better  circulation  in  the  arterial 
system,  since  it  is  in  this  respect  that  evils  arise. 

Cardio-vascular  derangements  are  to  be  combated  in  the  same 
manner  as  disorders  due  primarily  to  cardiac  insufficiency,  and 
these  do  not  need  to  be  repeated.  I  should  like  to  urge  the  neces- 
sity, however,  of  freely  using  vaso-dilators,  as  the  nitrites,  that  if 
possible  the  arterial  paths  may  be  somewhat  opened  up  and  the 
labour  of  the  left  ventricle  thereby  lessened.  In  this  class  of  cases 
nitroglycerin,  etc.,  should  always  be  given  whenever  it  is  necessary 
to  resort  to  digitalis.  It  is  because  of  the  constricting  action  of 
digitalis  on  the  arterioles  that  strophanthus  ought  to  be  tried 
instead,  and  only  replaced  by  digitalis  when  it  has  proved  in- 
efficient. 

Nothing  is  of  greater  service  in  cases  of  diffuse  arteriosclerosis 
with  secondary  venous  engorgement  than  a  periodic  purge  by 
means  of  calomel.  The  catharsis  should  be  brisk  to  be  of  benefit, 
for  relief  does  not  follow  until  several  watery  stools  have  been 
secured.  I  have  seen  truly  surprising  results  from  such  simple 
treatment.  One  instance  in  particular  comes  to  mind  as  I  write, 
that  of  an  old  German  with  very  stiff  vessels  who  exhausted  both 
my  patience  and  my  resources  in  a  vain  endeavour  to  procure  relief 
from  formication  and  coldness  of  the  thighs.  At  last,  in  despair, 
I  prescribed  5  grains  each  of  calomel  and  jalap  for  the  purpose  of 
preventing  his  return  to  my  clinic.  He  did  not  reappear  for  two 
or  three  months,  when  one  day  he  returned,  and  on  entering  the 
clinic  room  exclaimed  that  he  had  come  back  for  another  powder, 
as  he  had  never  had  anything  do  him  so  much  good. 

I  recall  also  an  Irishman  with  stiff  arteries  and  an  obstinate 
chronic  bronchitis  that  had  defied  the  efforts  of  several  well-known 
practitioners,  and  who  obtained  greater  relief  from  his  dyspnoea 
and  cough  by  a  single  dose  of  5  grains  of  calomel  than  from  all 
the  cough  anixtures  he  had  previously  taken. 

Traenkel  reports  the  highly  interesting  and  instructive  case 


758  DISEASES  OF  THE  HEART 

of  a  man  with  general  arteriosclerosis  who  was  relieved  of  his 
nocturnal  asthma  for  a  period  of  three  months  by  a  single  sharp 
attack  of  epistaxis.  This  suggests  that  in  cases  of  cardiac  asthma, 
which  so  often  form  a  distressing  feature  in  the  clinical  history  of 
arteriosclerosis  of  the  cardio-vascular  type,  it  might  be  well  to 
resort  to  venesection  when  catharsis  has  failed  of  ameliorating  the 
symptom. 

In  cerebral  arteriosclerosis  I  am  of  the  opinion  that  stimulants 
and  vaso-dilators  are  indicated.  Judgment  and  caution  should  be 
exercised  in  their  administration,  however,  lest  the  heart  be  too 
vigorously  stimulated  and  rupture  of  a  miliary  aneurysm  result. 
The  safety  of  such  medication  may  be  estimated  by  the  state  of  the 
cardiac  muscle.  They  are  certainly  indicated  when  the  systoles  are 
feeble  and  the  brain  is  not  sufficiently  flushed. 

The  treatment  of  coronary  sclerosis  and  its  resulting  angina 
pectoris  has  already  been  considered  in  the  chapters  on  Chronic 
Myocarditis  and  Angina  Pectoris. 

The  management  of  renal  sclerosis  is  essentially  that  of 
chronic  nephritis,  since  the  two  conditions  are  so  frequently  com- 
bined. When  vascular  disease  in  the  extremities  has  led  to  gan- 
grene, the  treatment  is  of  necessity  surgical.  Sclerosis  of  the  pul- 
monary artery  is  practically  that  of  arteriosclerosis  in  general  plus 
that  of  bronchitis  and  emphysema. 

Only  general  principles  can  here  be  laid  down.  In  every  case 
special  symptoms  must  be  left  to  the  judgment  of  the  practitioner. 


CHAPTER    XXXIII 

ACUTE  AORTITIS- ACUTE  ARTERITIS  -  SYPHILITIC 
ARTERITIS-ENDARTERITIS  OBLITERANS-PERI AR- 
TERITIS NODOSA-STENOSIS  OF  THE  AORTA  AND 
PULMONARY  ARTERY-CONGENITAL  SMALLNESS 
OF    THE    ARTERIES 

I.  ACUTE  AORTITIS 

When  acute  inflammation  of  the  aorta  is  discovered  it  is  in 
most  cases  associated  with  the  changes  of  sclerosis  in  the  same  situ- 
tion  or  with  an  acute  endocarditis.  French  authors,  however,  have 
described  a  form  of  acute  aortitis  which  they  claim  is  independent 
of  antecedent  sclerotic  change  and  occurs  in  the  course  of  acute 
infectious  diseases.  Such  statements  are  received  with  consider- 
able reserve  by  the  Germans,  and  von  Schroetter  in  jSTothnagel's 
System  seems  quite  sceptical  on  the  subject,  particularly  as  regards 
its  clinical  recognition. 

Morbid  Anatomy. — The  aorta  is  found  more  or  less  dilated, 
and  the  surface  of  the  intima  looks  rough  from  the  presence  of 
reddish  or  grayish  translucent  more  or  less  thickly  scattered 
patches  of  a  gelatinous  consistency.  These  are  minute  thrombi, 
and  it  is  through  the  detachment  of  these  that  cutaneous  and  other 
infarcts  occur,  the  same  as  in  acute  valvulitis.  Indeed,  acute  aor- 
titis is  so  similar  to  acute  endocarditis  that  the  description  of  the 
latter  may  answer  for  the  former. 

The  process  may  be  of  a  benign  type  and  proceed  to  the  forma- 
tion of  so-called  vegetations,  or  it  may  behave  like  ulcerative  endo- 
carditis and  lead  to  serious  destruction  of  the  vessel  and  rupture. 
In  this  manner  communication  may  be  established  between  the 
aorta  and  one  of  the  auricles,  a  contiguous  vessel  or  the  pericar- 
dium with  fatal  haemorrhage  (Romberg).  The  media  and  even 
the  adventitia  becomes  infiltrated  with  round  cells,  and  if  the  pro- 

759 


760  DISEASES  OF  THE  HEART 

cess  is  sufficiently  prolonged  newly  formed  vessels  may  penetrate 
into  the  intima. 

As  already  stated,  degenerative  changes  are  usually  found  as- 
sociated with  the  evidences  of  acute  inflannnation.  There  may 
also  be  an  associated  valvulitis  affecting  previously  healthy  valves 
or  more  often  as  an  acute  process  ingrafted  on  an  old-standing 
aortic-valve  lesion.  In  other  distant  parts  of  the  body  there  may 
be  discovered  local  changes  due  to  benign  or  septic  emboli  cast  off 
from  the  aortic  intima. 

Etiology. — The  aorta  may  become  acutely  inflamed  in  conse- 
quence of  direct  extension  of  an  identical  process  of  the  endocar- 
dium. French  clinicians  (Huchard,  Leger,  Siredi,  etc.)  maintain 
that  acute  aortitis  may  arise  in  the  course  of  scarlatina,  measles, 
variola,  independently  of  involvement  of  the  endocardium,  and 
Fiessinger  is  said  to  have  seen  it  in  a  case  of  influenza  (Gibson). 
The  latter  says  also  that  acute  aortitis  may  be  associated  with  acute 
pneumonia,  pleurisy,  and  pericarditis.  The  disease  has  also  been 
attributed  to  trauma,  and  has  been  observed  in  the  course  of  chronic 
nephritis. 

Symptoms. — Acute  aortitis  in  most  instances  is  latent  or  is 
overlooked  by  reason  of  its  occurrence  in  the  course  of  some  other 
distinctive  affection.  The  case  discovered  by  Thoma,  and  which 
occurred  during  measles,  had  produced  no  symptoms  whatever. 
Von  Schroetter  appears  to  think  that  the  clinical  features  de- 
scribed by  Huchard  in  such  a  brilliant  and  interesting  fashion  are 
not  to  be  attributed  to  acute  aortitis  per  se,  but  are  such  as  are 
so  often  observed  in  cases  of  arteriosclerosis  affecting  the  aortic 
arch.  In  Chapter  IV,  page  158,  I  have  depicted  a  case  which  I 
took  to  be  acute  endocarditis  because  of  the  subjective  symptoms 
and  clinical  findings,  and  in  which  post-mortem  examination  dis- 
closed an  aortitis  together  with  endocarditis,  the  acute  process  hav- 
ing developed  on  top  of  old  sclerotic  changes  that  had  masqueraded 
under  the  guise  of  aortic  insufficiency. 

I  will  briefly  portray  the  features  that  are  claimed  by  the 
Frencli  t(»  liave  been  observed  in  acute  aortitis  unconnected  with 
other  aortic  or  endocardial  lesions.  Fever  is  usually  absent,  but  if 
present  it  is  due  to  the  primary  infection,  not  to  tlic  aortitis  as  such. 
The  countenance  is  apt  to  be  pale  and  anxious.  The  pulse  is  small 
and  weak,  regular  or  not,  as  circumstances  in  each  case  may  die- 


ACUTE  AORTITIS  761 

tate.  The  patient  is  likely  to  complain  of  pain  in  the  upper  ster- 
nal region,  and  sometimes  extoiidiiig  through  the  mediastinum 
and  down  the  back  along  the  spinal  column.  The  pain  is  described 
as  burning,  sticking,  smarting,  etc.,  and  in  some  instances  is  said  to 
radiate  into  the  left  shoulder  and  down  the  arm,  very  like  that  of 
angina  pectoris.  The  resemblance  to  this  latter  is  enhanced  by  a 
feeling  of  oppression  and  anxiety  in  some  cases. 

Peter  has  observed  tenderness  on  pressure  in  the  intercostal 
spaces  to  the  left  of  the  manubrium,  and  undue  throbbing  of  the 
right  subclavian  has  been  noted  by  French  writers  (Laboulbene, 
Faure),  and  by  them  is  attributed  to  the  greater  liability  to  in- 
flammation of  the  left  subclavian  than  of  the  innominate  artery. 
Von  Schroetter,  however,  believes  that  if  such  difference  in  the 
pulsation  of  the  two  subclavia  exists,  it  is  due  to  sclerotic  changes, 
an  opinion  in  which  Gibson  concurs. 

Dysphagia,  cough  with  expectoration,  and  disturbance  of  the 
digestive  tract  shown  by  vomiting  and  flatulent  distention  of  the 
bowels,  have  been  observed  in  some  cases. 

In  short,  the  symptoms  of  this  affection  are  often  wholly  want- 
ing, and  when  present  are  not  at  all  distinctive.  There  is  noth- 
ing in  them  which  may  not  be  observed  in  other  affections  involv- 
ing the  heart,  and  hence  Romberg  states  that  even  when  the  malig- 
nant form  of  acute  aortitis  occurs,  there  is  nothing  in  its  clinical 
picture  to  distinguish  it  from  ulcerative  endocarditis. 

The  course  of  acute  aortitis  is  often  protracted  and  the  termi- 
nation is  usually  in  death. 

Physical  Signs  are  usually  indefinite,  or  are  such  as  are 
found  in  other  acute  inflammations  involving  the  cardiac  struc- 
tures, or  are  those  of  the  infection  in  the  course  of  which  acute 
aortitis  occurs. 

Inspection. — The  countenance  may  be  pallid  and  anxious,  the 
carotids  throb  strongly,  and  the  right  subclavian  may  pulsate  more 
powerfully  than  does  the  left. 

Palpation  is  negative  unless  pressure  elicits  sensitiveness  in  the 
intercostal  spaces  to  left  of  the  sternum  and  along  the  course  of  the 
aorta. 

Percussion  is  likely  to  be  negative  unless  dulness  be  revealed  at 
right  of  the  manubrium  in  cases  in  which  the  inflammation  leads 
to  dilatation  of  the  aortic  arch. 


762  DISEASES  OF  THE   HEART 

Auscultation. — This  is  not  likely  to  furnish  information  of  a 
positive  kind.  A  systolic  murmur  over  the  situation  of  the  ascend- 
ing arch  may  be  evoked  by  dilatation  of  the  vessel,  and  in  cases  in 
which  the  valve  is  also  affected  there  may  be  impurity  of  the  aortic 
second  tone. 

Diagnosis. — This  can  rarely  if  ever  be  more  than  conjectural. 
If  the  character  of  the  pain  and  oppression  simulate  that  of  angina 
pectoris,  it  may  possibly  be  differentiated  from  it  by  the  fact  that 
in  acute  aortitis  this  symptom  is  likely  to  persist,  or  at  the  most 
show  only  remissions,  not  intermissions. 

The  differentiation  from  acute  endocarditis  is  not  possible  in 
all,  perhaps  not  in  most  cases.  Aid  may  be  obtained,  however,  if 
one  notes  that  in  the  course  of  a  disease  resembling  endocarditis 
no  changes  in  the  area  of  cardiac  dulness  or  in  the  heart-sounds 
are  developed,  or  if  on  repeated  examinations  one  should  be  able 
to  detect  increasing  dulness  over  the  ascending  aorta  indicative  of 
dilatation.  In  my  case  this  was  noticed,  but  was  not  correctly  in- 
terpreted, owing  perhaps  to  the  coincident  dilatation  of  the  right 
auricle. 

Prognosis. — This  may  be  said  to  be  very  unfavourable.  The 
occurrence  of  embolic  phenomena  renders  the  outlook  most  un- 
promising. Rupture  of  the  aorta  is  a  possibility  that  should 
always  he  borne  in  mind  in  suspected  cases  of  the  disease. 

Treatment  cannot  be  expected  to  do  more  than  relieve  symp- 
toms. Rest  in  bed  is  imperatively  indicated,  and  the  strength  of 
the  patient  must  be  sustained  by  highly  nourishing,  easily  digested 
food.  Pain,  when  severe,  should  be  allayed  by  morphine,  counter- 
irritation,  hot  applications,  etc.  Nitroglycerin  may  be  of  service 
by  diminishing  intra-aortic  blood-pressure,  and  strychnine  is  a  val- 
uable general  and  cardiac  tonic.  Digitalis  is  only  useful  in  case 
of  threatening  cardiac  inadequacy. 

II.  ACUTE  ARTERITIS 

Morbid  Anatomy.  —  Circumscribed  inflammation  of  the 
larger  arteries  is  sometimes  observed  in  connection  with  an  in- 
flammatory process  of  surrounding  tissues  or  in  consequence  of 
embolic  plugging.  Infiltration  with  small  round  cells  takes  place 
in  the  outer  and  middle  coats,  later  on  also  in  the  intima.  The 
endothelial  lining  becomes  swollen   and   of  increased  thickness, 


ACUTE  ARTERITIS  763 

while  the  underlying  layers  of  the  intima  show  the  development 
of  newly  formed  connective  tissue. 

In  cases  in  which  the  inflammation  is  the  result  of  plugging, 
thrombosis  also  occurs,  and  in  time  the  thrombus  undergoes  organ- 
ization. If  the  embolus  is  infective,  the  inflammation  may  spread 
to  the  parts  outside  of  the  vessel  and  set  up  abscess.  When  the 
arteritis  results  from  surrounding  inflammation,  thrombosis  and 
subsequent  organization  may  likewise  take  place. 

The  etiology  has  already  been  stated  in  the  opening  sen- 
tence. Acute  arteritis  results  either  from  adjacent  inflammation 
or  from  embolic  occlusion. 

Symptoms  are  likely  to  be  recognised  only  when  the  arteritis 
is  situated  in  an  extremity  or  a  part  accessible  to  palpation,  and 
when  thereby  one  can  detect  either  embolism  or  thrombosis,  or 
when  there  is  phlegmonous  inflammation  of  the  tissues  surround- 
ing an  artery  of  considerable  size. 

When  local  inflammation  invades  the  artery,  involvement  of 
the  latter  is  likely  to  be  masked  by  the  symptoms  of  associated 
phlebitis.  In  the  latter  event  there  are  circulatory  disturbances 
due  to  interference  with  return  flow,  swelling,  and  more  or  less 
oedema,  together  with  pain  and  great  tenderness. 

In  the  case  of  embolism  there  are  pain  and  phenomena  of 
obstructed  circulation,  coldness  (local  syncope),  cyanosis,  and 
numbness. 

Physical  Signs  consist  of  such  phenomena  of  local  inflam- 
mation or  of  the  accompanying  phlebitis. 

Inspection  perceives  swelling  and  redness  of  the  affected  ex- 
tremity. 

Palpation  is  of  greater  service.  The  limb  is  hot,  painful  to 
touch,  usually  pits  on  pressure,  and  at  some  point  careful  palpa- 
tion is  generally  able  to  detect  resistance  due  to  the  embolus  or  to 
thrombosis  extending  for  a  variable  distance  above  the  seat  of  the 
plug. 

Diagnosis. — This  is  to  be  made  by  the  history,  local  symp- 
toms, and  the  result  of  palpation.  The  differentiation  of  acute 
arteritis  from  phlebitis  is  not  always  easy  or  possible. 

Prognosis  depends  upon  the  nature  of  the  cause  and  the 
completeness  of  collateral  circulation.  Acute  meningitis  is  a  pos- 
sibility in  certain  cases,  and  of  course  affords  a  very  grave  outlook. 


764  DISEASES  OP  THE  HEART 

The  prognosis  is  always  unfavourable  in  cases  in  which  the  arte- 
ritis is  secondarv  to  acute  uuilignant  endocarditis. 

The  treatment  of  acute  arteritis  is  partly  medical  and  partly 
surgical.  The  affected  limb  should  be  elevated,  kept  at  absolute 
rest,  and  enveloped  in  moist  heat,  as  poultices  to  which  anodyne 
remedies  may  have  been  added.  Pain  is  to  be  allayed  by  local 
sedatives  or  by  the  use  of  opimn  in  some  form.  Should  an  abscess 
occur,  it  is  to  receive  appropriate  surgical  management. 

III.   SYPHILITIC  ARTERITIS 

Vascular  changes  observed  in  syphilitic  subjects  have  been  the 
object  of  careful  study  by  numerous  investigators,  among  whom 
should  be  mentioned  Lanccreaux,  ITeubner,  Weigert,  Doelile, 
Baumgarten,  Vendeler.  Some  of  the  changes  are  unquestionably 
of  luetic  origin,  while  others  are  by  some  authors,  as  von  Schroet- 
ter,  accepted  with  considerable  doubt. 

Morbid  Anatomy. — The  inflammatory  changes  in  the  arter- 
ies are  of  a  chronic  nature  and  invade  circumscribed  portions  of  a 
vessel  or  are  limited  to  the  arteries  of  certain  regions,  as  of  the 
brain.  The  process  may  show  itself  as  circumscribed  patches  of  a 
grayish  white  translucent  appearance,  or  the  entire  vessel  may  be 
changed  into  a  whitish  or  grayish  cord  in  consequence  of  the  trans- 
formation of  its  coats  into  fibrous  tissue.  In  this  form  the  adven- 
titia,  and  ultimately  the  media  and  intima,  become  infiltrated  with 
round  or  fusiform  cells.  The  process  may  remain  in  this  stage  of 
inflammatory  infiltration  (von  Schroetter),  but  as  a  rule  it  goes 
on  to  formation  of  fibrous  tissue  in  the  several  coats. 

This  hyperplasia  of  the  walls  is  often  extreme  and  leads  to 
very  considerable  narrowing  and  even  occlusion  of  the  lumen  of 
the  artery. 

In  this  respect  syphilitic  arteritis  difl'ers  from  arteriosclerosis, 
which  is  more  apt  to  lead  to  dilatation  than  to  obliteration  of  a  ves- 
sel, although  it  may  do  this  latter  in  the  smallest  arteries. 

It  has  been  shown,  furthermore,  particularly  by  Baumgarten, 
that  minute  gummata  are  scattered  in  the  middle  coat  in  imme- 
diate proximity  to  the  vasa  vasorum.  Atrophy  and  rupture  of  the 
media  result,  and  in  time  the  rents  are  repaired  by  the  formation 
of  cicatricial  tissue.  The  subsequent  contraction  of  these  areas 
leads  to  pouchings  of  the  intima,  which,  when  they  are  found  in 


SYPHILITIC  ARTERITIS  T65 

the  ascending  aorta,  are  almost  pathognostic  of  syphilis  (Rom- 
berg). These  pouchings  of  the  aortic  intima  may  prove  the  start- 
ing-place of  future  aneurysms. 

In  another  form  of  arterial  disease  due  to  syphilis  the  vessel 
becomes  invaded  by  a  syphilitic  process  in  its  neighbourhood.  The 
vessel  is  surrounded  by  a  gummatous  mass  or  by  dense  cicatricial 
tissue,  and  the  coats  of  the  artery  are  more  or  less  thickened  and 
altered  (Ziegler).  In  the  early  or  inflammatory  stage  the  outer 
and  inner  coats  are  rich  in  cells,  but  as  the  process  advances 
fibrous  tissue  replaces  the  cells  wholly  or  in  part.  The  media 
is  not  so  much  invaded  by  fibrous  tissue  as  are  the  adventitia  and 
intima. 

The  cerebral  arteries  appear  to  be  the  ones  most  frequently 
affected.  The  aorta  and  coronary  arteries  may,  however,  be  the 
seat  of  syj^hilitic  disease,  and  in  a  few  cases  the  vessels  of  the 
extremities  have  been  affected.  C.  O.  Weber  is  said  by  von  Schroet- 
ter  to  have  found  the  right  branch  of  the  pulmonary  artery  in  a 
syphilitic  girl  greatly  narrowed  by  reason  of  a  gumma  in  its  wall. 
Zeissl  is  also  stated  by  the  same  author  to  have  found  the  left 
brachial  artery  invaded  by  a  gummatous  infiltration,  wdiile  Lang- 
enbeck  saw  the  same  sort  of  process  in  the  right  brachial  of  another 
case. 

Etiology. — Syphilitic  arteritis  is  a  late  manifestation  of  lues. 

The  symptoms  are  determined  by  the  seat  of  the  arteritis. 
In  the  case  of  the  brain  they  are  those  of  disturbed  or  obstructed 
circulation,"  loss  of  memory,  dizziness,  headache,  mental  confu- 
sion, epilepsy,  etc. — in  short,  such  as  arise  from  areas  of  acute 
softening. 

When  the  disease  affects  the  aorta  it  may  lead  to  aneurysm  or 
to  the  symptom-complex  of  sclerosis  of  the  arch. 

Arteritis  of  this  origin  may  be  a  cause  of  angina  pectoris  by 
leading  to  sclerosis  and  occlusion  of  the  coronaries,  particularly  the 
left  anterior  descending  branch.  In  very  rare  instances  a  coronary 
artery  has  been  said  to  be  invaded  and  obliterated  by  a  gumma  of 
the  myocardium. 

In  the  extremities  syphilitic  arteritis  occasions  clinical  mani- 
festations of  obstructed  circulation  the  same  as  may  other  forms 
of  arterial  disease,  pallor  or  cyanosis,  coldness,  and  eventually 
gangrene. 


766  DISEASES  OF  THE  HEART 

Tlic  diagnosis  must  depend  upon  the  history  of  hietic  infec- 
tion and  on  the  discovery  of  unmistakable  lesions  indicating  a  late 
staiic  of  the  disease.  Even  in  such  a  case  one  cannot  always  say 
positively  that  the  vascular  changes  observed  are  of  specific  origin. 
They  may  be  due  to  arteriosclerosis  and  be  independent  of  syphilis 
per  se.  In  some  cases  one  may  be  obliged  to  await  the  result  of 
treatment  before  being  able  to  arrive  at  a  definite  diagnosis. 

The  prognosis  is  not  always  favourable  as  regards  recovery, 
although  appropriate  therapy  may  in  some  cases  affect  a  restora- 
tion of  health.  If  the  arteritis  has  led  to  pronounced  fibrous  thick- 
ening and  considerable  obstruction,  to  pouching,  or  even  to  aneu- 
rysm, there  is  small  prospect  of  favourably  influencing  the  process 
by  antisyphilitic  medication  no  matter  how  vigorous. 

The  treatment  should  consist  of  the  administration  of  ap- 
proved specific  remedies — i.  e.,  mercury  and  iodides.  In  addition, 
one  may  have  to  treat  certain  symptoms,  as  angina  pectoris,  cardiac 
inadequacy,  gangrene,  cerebral  disorders,  etc.  The  management 
of  aortic  aneurysm  will  be  found  in  a  succeeding  chapter. 

IV.  ENDARTERITIS  OBLITERANS 
The  following  account  is  a  condensed  statement  taken  from 
von  Schroetter's  excellent  description  of  the  disease  in  Notli- 
nagel's  Specielle  Pathologic  und  Therapie.  No  apology  for  such 
a  transcript  is  necessary,  since  the  disease  in  question  is  rare,  and 
comparatively  few  contributions  to  the  subject  have  been  made. 
The  designaticm  obliterans  was  suggested  by  Winiwarter,  whose 
case  is  considered  so  typical  by  von  Schroetter  that  he  makes  use 
of  Winiwarter's  description.  Billroth  gave  it  the  name  Ilyper- 
plastica,  while  Orth  called  it  Productiva.  Other  observers  to 
whose  views  or  cases  von  Schroetter  refers  are  Weiss,  Brochard, 
Schlesinger,  Sternberg,  Wiedermann,  Ortmann,  Hadden,  Gold- 
flam,  Welter,  (\>ll('t,  Thatin,  Roque,  Braun. 

Morbid  Anatomy. — The  disease  occurs  most  often  in  the 
smaller  arteries  of  the  foot  or  leg,  occasionally  also  in  the  upper 
extremity,  and  exceptionally  in  other  parts.  Upon  macroscopic 
inspection  the  vessels  are  seen  to  be  enveloped  by  a  tough  fibrous 
sheatli  wliich  binds  them  firmly  together.  The  individual  artery 
— e.  g.,  posterior  tibial — is  converted  into  a  firm  whitish  cord,  and 
on  section  is  seen  to  be  filled  with  a  whitish  gray  or  grayish  brown 


ENDARTERITIS  OBLITERANS  7G7 

mass,  so  that  a  probe  can  be  passed  into  the  vessel  only  with  diffi- 
culty or  not  at  all. 

The  artery  is  nevertheless  not  uniformly  so  filled,  yet  on  the 
whole  is  transformed  into  a  rigid  cord  in  consequence  of  its  inte- 
rior being  filled  with  a  somewhat  yielding  wide-meshed  tissue. 
The  process  begins  at  the  jDcriphery  and  extends  upward,  reaching 
from  the  plantar  peroneal  and  posterior  tibial  arteries,  even  in 
some  instances  to  the  femoral,  or  in  the  case  of  the  arm,  to  the 
brachial. 

Histological  examination  reveals  in  different  places  a  somewhat 
variable  condition,  yet  which  is  in  reality  a  hyperplasia  of  the 
intima  which  may  augment  its  thickness  to  even  eight  times  the 
normal.  In  the  larger  vessels  the  newly  formed  connective  tissue 
is  composed  of  round,  spindle-shaped,  or  stellate  cells,  between 
which  can  be  recognised  an  intercellular  substance  made  up  of 
delicate  threads.  According  to  Winiwarter  and  others,  several 
strata  of  elastic  fibres  may  be  seen  in  the  outer  portion  of  the  in- 
tima next  to  the  media.  Finally,  minute  blood-vessels  are  seen  to 
exist  within  the  connective  tissue  of  the  interior,  which  Winiwarter 
regards  as  an  extension  or  formation  of  new  channels  by  which  an 
attempt  is  made  to  provide  a  collateral  circulation,  and  not  as  an 
organization  of  a  thrombus.  The  capillaries  thus  formed  permit 
a  partial  injection  of  the  mass  filling  up  the  lumen  of  the  artery. 
In  spite  of  this  attempt  at  a  collateral  circulation  the  stump  after 
an  amputation  does  not  bleed  freely  when  the  Esmarch  bandage 
is  removed. 

Etiology. — This  is  practically  unknown.  It  has  been  ob- 
served in  men  far  more  frequently  than  in  w^omen,  and  what  is 
especially  strange  about  it  is  that  it  attacks  comparatively  young 
and  previously  healthy  individuals.  The  process  does  not  neces- 
sarily invade  all  the  arteries  of  a  limb,  for  it  has  been  found  in 
the  posterior  tibial,  while  the  anterior  tibial  was  free.  It  has  been 
attributed  to  occupation,  but  in  von  Schroetter's  opinion  without 
sufficient  warrant.  The  only  theory  that  seems  to  appeal  to  von 
Schroetter  is  that  the  affection  is,  in  some  manner  as  yet  unknown, 
dependent  on  some  nervous  influence. 

Symptoms  are  made  up  of  prodromata  extending  through  a 
period  of  years,  as  many  as  twelve,  and  of  such  phenomena  as 
depend  upon  interference  with  local  circulation.    Individuals  thus 


768  DISEASES  OP  THE  HEART 

afflicted  complain,  for  years  of  pains  in  the  leg  or  arm  Avhicli  are 
generally  thought  to  be  either  rheumatoid  or  neuralgic,  and  are 
likely  to  be  treated  as  such,  yet  without  benefit. 

After  a  time  perversions  of  sensation  occur  (parsesthesiae), 
as  formication,  numbness,  etc.  At  first  the  pains  are  lessened 
or  disappear  when  the  extremity  is  at  rest,  but  at  length 
grow  extreme,  and  on  use  of  the  affected  member  become  intoler- 
able. As  the  obstruction  to  circulation  increases  movement  be- 
comes difficult  and  the  extremity  feels  heavy,  so  that  the  patient 
favours  the  limb  so  far  as  possible  and  may  actually  walk  lame. 

When  at  last  the  artery  is  wholly  occluded  areas  of  gangrene 
make  their  appearance.  These  may  be  superficial  or  may  invade 
a  toe  or  the  whole  foot,  and  show  a  tendency  to  sj)read  rajDidly 
upward.  The  extremity  now  looks  either  pale  or  livid  and  feels 
cold  and  lifeless.  Unless  the  gangrenous  area  is  removed  by  the 
surgeon  septic  phenomena  may  develop  and  lead  to  a  fatal  termi- 
nation of  the  case.  The  course  of  the  disease  is  progressive,  and 
the  termination  is  usually  or  invariably  fatal  in  the  course  of 
years. 

The  diagnosis  is  surrounded  by  considerable  difficulty,  par- 
ticularly in  tlio  prodromal  stage.  The  pains  are  likely  to  be  con- 
sidered rheumatic  or  simply  neuralgic,  and  cannot  very  well  be 
correctly  interpreted  before  there  is  evidence  of  rigidity  of  and 
want  of  pulsation  in  the  arteries. 

Obliterating  endarteritis  is  to  be  distinguished  from  arterio- 
sclerosis mainly  by  the  age  of  the  patient,  since  it  has  been  observed 
most  frequently  between  twenty  and  thirty,  next  between  forty 
and  fifty,  and  arteriosclerosis  occurs  most  often  past  fifty.  The 
disease  is  likely  to  be  localized,  while  evidence  of  vascular  degen- 
eration is  usually  more  wide-spread.  Moreover,  arteriosclerosis, 
althougli  it  may  cause  gangrene,  does  so  far  less  constantly  than 
does  the  endarteritis,  and  then  usually  in  persons  who  present 
well-marked  evidence  of  the  arterial  change  in  both  legs. 

Reynaud's  disease,  for  which  the  endarteritis  may  be  mistaken, 
occurs  most  frequently  in  children  and  young  adults,  especially  in 
females,  sets  in  al)ru})tly,  and  the  dead  feeling  of  the  fingers  of  both 
hands  is  attended  with  slight  annesthesia.  Moreover,  the  condition 
is  due  to  a  cramplike  constriction  of  the  vessels,  and  is  not  attended 
with  rigidity  and  pulselessness  of  the  vessels. 


PERIARTERITIS  NODOSA  769 

The  prognosis    is  imf avourablc,  since  the  affection  is  pro- 


gressive. 


Treatment  is  of  a  necessity  symptomatic  and  restricted  to 
such  measures  as  may  alleviate  suffering.  The  occurrence  of  gan- 
grene calls  for  surgical  interference. 

V.  PERIARTERITIS  NODOSA.     SYN.:   CONGENITAL   ANEURYSM 

The  very  remarkable  and  rare  affection  which  bears  the  above 
titles  was  first  adequately  described  by  Kussmaul  and  Maier  in 
1866,  although  it  appears  that  Rokitansky  in  1852,  and  possibly 
Pelletan  in  1810,  observed  each  a  single  case  (von  Schroetter). 
The  designation  Periarteritis  Nodosa  w^as  bestowed  upon  it  by 
Kussmaul  because  of  his  conception  of  the  process  as  an  inflam- 
mation originating  in  the  adventitia.  The  term  Congenital  Aneu- 
rysm is  applied  to  it  because  it  has  been  thought  to  be  due  to  con- 
genital weakness  of  the  arterial  coats  (Eppinger),  leading  event- 
ually to  the  development  of  multiple  aneurysms.  According  to 
von  Schroetter,  only  thirteen  authentic  cases  have  been  reported. 

Morbid  Anatomy. — The  affected  artery  is  studded  with 
nodular  thickenings  of  a  whitish  colour  and  of  variable  size,  from 
that  of  a  pin's  head  to  a  pea,  which  are  due  to  circumscribed  fibrous 
thickening  of  the  intima  with  cellular  infiltration  of  the  adven- 
titia and  media.  The  lumen  of  the  vessel  may  be  narrowed  or 
the  weakening  of  its  coats  may  lead  to  circumscribed  dilatations — 
i.  e.,  multiple  aneurysms.  These  may  reach  such  numbers  as  to  be 
uncountable.  The  disease  affects  arteries  of  medium  calibre,  and 
is  found  with  special  frequency  in  the  arteries  of  the  muscles  and 
viscera,  as  the  heart,  intestines,  spleen,  liver,  and  kidneys,  and 
also  of  the  skin. 

Its  etiology  is  entirely  unknown,  but  inasmuch  as  the  clin- 
ical picture  is  very  like  that  of  sepsis  or  an  infection  it  may  have 
some  such  origin  (Romberg).  The  disease  appears  to  attack  both 
sexes  about  equally  and  to  occur  between  the  ages  of  twenty  and 
fifty-two  (Osier). 

Symptoms. — The  most  striking  features  of  the  affection  are 

weakness,  rapidly  progressing  ana?mia,  and  rapidity  of  the  pulse 

out  of  all  proportion  to  the  temperature.    Fever  may  be  present  in 

the  beginning,  but  is  of  moderate  height,  and  tends  to  ultimately 

disappear.     There  is  pain  in  the  muscles  which  may  eventually 
50 


770  DISEASES  OF  THE   HEART 

show  atrophic  changes  and  paralysis.  Digestive  disturbances  are 
present,  as  anorexia,  thirst,  and  vomiting,  and  there  may  be  con- 
stipation or  diarrh(pa.  There  may  be  albuminuria  and  casts,  and 
when  the  arteries  of  the  abdominal  organs  are  affected  there  is 
severe  epigastric  distress.  Iljemorrhages  from  the  bowel  may  also 
be  observed  (Romberg)  in  cases  in  which  the  arteries  of  the  intes- 
tines are  the  seat  of  the  disease. 

The  course  of  the  malady  is  progressive  as  a  rule,  and  a  fatal 
termination  occurs  in  from  six  weeks  to  three  months.  Very  ex- 
ceptionally, however,  recovery  may  ensue. 

Diagnosis  is  impossible  unless  the  nodular  thickenings  can 
be  felt  along  the  course  of  peripheral  arteries  or  such  as  situated 
within  the  abdomen  are  yet  accessible  to  palpation.  In  suspected 
cases  a  nodule  may  be  excised  and  subjected  to  microscopic  exami- 
nation. 

Prognosis  is  unfavourable,  although  recovery  does  not  appear 
to  be  impossible. 

Treatment  is  purely  symjitomatic  and  is  limited  to  attempts 
to  alleviate  suffering,  build  up  strength,  and  check  or  overcome  the 
destruction  of  the  blood. 

VI.  STENOSIS  OF   THE  AORTA   AND   PULMONARY  ARTERY 

Stenosis  of  the  Aorta  may  be  Congenital  or  Acquired. — In  the 
former  variety  the  narrowing  is  situated  at  the  isthmus  and 
may  be  caused  by  a  too  early  closure  of  Botalli's  duct  and  conse- 
quent failure  of  the  descending  aorta  to  receive  the  amount  of 
blood  necessary  for  its  proper  development  or  expansion,  or  a 
membrane  may  be  stretched  across  the  vessel  at  the  isthmus,  having 
at  its  centre  an  opening  through  which  the  stream  of  blood  must 
pass. 

Acquired  stenosis  may  be  caused  l)y  a  fibrous  band  that  con- 
stricts the  aorta  at  some  point  within  the  mediastinum,  or  it  may 
be  compressed  by  a  tumour.  Such  conditions  are,  however,  rare 
as  regards  the  arch,  since  this  portion  of  the  aorta  is  capable  of 
successfully  withstanding  en(;roachment  upon  it  by  new  growths 
(Romberg). 

In  the  chapter  on  Dextrocardia  is  lucntioncd  the  case  of  a  child 
in  whom  the  rotation  and  displacement  of  the  heart  had  caused 
the  superior  vena  cava  to  be  stretched  tightly  across  the  aorta  and 


STENOSIS   OF   THE   AORTA   AND  PULMONARY   ARTERY      771 

constrict  its  lumen.  I  have  also  in  the  chapter  on  Aortic  Regurgi- 
tation mentioned  the  case  of  a  man  whose  ascending  aorta  was 
greatly  narrowed  by  a  ring  of  fibrous  tissue  that  completely 
encircled  the  vessel  and  had  induced  relative  insufficiency  of  the 
valve. 

Symptoms  depend  upon  the  degree  and  seat  of  the  stenosis. 
In  the  congenital  form  collateral  circulation  may  become  estab- 
lished through  the  intercostal  arteries,  the  internal  mammary,  or 
arteries  in  the  integument  and  muscles  of  the  back.  If  such  side 
channels  are  sufficient  there  may  be  no  obvious  hindrance  to  the 
blood-supply  of  the  lower  parts  of  the  body,  and  no  untoward 
effects  are  experienced. 

Romberg  mentions  a  case  observed  by  him  in  which  the  arter- 
ies of  the  back  provided  a  means  of  maintaining  the  circulation 
below  the  point  of  stenosis,  and  in  which  he  detected  a  loud  vascu- 
lar bruit  on  the  posterior  aspect  of  the  trunk  between  the  vertebral 
column  and  right  scapula.  The  murmur  was  attributed  by  him  to 
dilatation  of  the  arteries  at  that  point. 

In  the  acquired  form  narrowing  of  the  aorta  is  likely  to  occa- 
sion compensatory  hypertrophy  of  the  left  ventricle  and  possibly 
also  incompetence  of  the  aortic  valve,  as  in  my  case.  The  ulti- 
mate effects  are  those  of  cardiac  inadequacy.  In  cases  in  which 
relative  insufficiency  does  not  occur,  but  the  stenosis  leads  to  left- 
ventricle  hypertrophy,  the  clinical  history  is  likely  to  be  that  of 
narrowing  of  the  ostium  or  of  the  disease  which  causes  the  con- 
striction of  the  aorta. 

The  diagnosis  is  very  difficult  as  a  rule,  and  may  be  impos- 
sible. One  may  recognise  the  signs  of  obstruction  to  outflow  from 
the  ventricle,  but  may  not  be  able  to  determine  its  real  nature. 
The  detection  of  a  mediastinal  tumour  or  of  chronic  fibrous  medi- 
astinitis,  together  with  the  signs  of  obstruction — i.  e.,  a  systolic 
bruit  over  the  course  of  the  aortic  arch  with  accentuation  of  the 
aortic  second  tone  and  left-ventricle  hypertrophy — might  lead  to  a 
correct  diagnosis.  This  would  be  strengthened  if  as  time  went  on 
evidence  of  regurgitation  should  appear. 

Congenital  narrowing  of  the  isthmus  might  be  diagnosed  if  one 
were  to  discover  compensatory  dilatation  of  the  arteries  by  which 
collateral  flow  is  established  together  with  hypertrophy  of  the  left 
ventricle.  • 


772  DISEASES   OF  THE   HEART 

Prognosis  depends  upon  the  cause  and  degree  of  the  stenosis, 
the  effects  on  the  heart,  and  in  congenital  cases  the  completeness 
of  collateral  circulation.  The  general  health  may  not  be  seriously 
influenced,  or  the  heart  may  suifer  in  its  integrity,  and  death  be 
ultimately  brought  about  through  cardiac  inadequacy.  In  a  few 
cases  the  prognosis  may  be  that  of  the  etiological  condition. 

Treatment  is  to  be  addressed  to  obviating  so  far  as  possible 
the  injurious  consequences  of  the  acquired  stenosis.  We  can  do 
nothing  towards  removing  the  cause. 

Stenosis  of  the  Pulmonary  Artery  is  acquired,  and  is  a  relatively 
infrequent  condition.  It  may  be  due  to  constriction  by  a  fibrous 
band,  to  compression  by  an  aortic  aneurysm  and  a  few  other  con- 
ditions, of  wliich  isolated  examples  have  been  reported.  Thus 
Romberg  states  that  Litten  found  stenosis  of  the  pulmonary  artery 
from  an  "  echinococcus  embolus,"  while  Gerhardt  discovered  a  case 
of  slight  compression  of  the  vessel  by  the  left  auricle  in  conse- 
quence of  this  having  become  distended  by  a  clot.  C.  O.  Weber, 
cited  by  von  Schroetter,  observed  pronounced  narrowing  of  this 
artery  by  a  bean-shaped  gumma  in  its  wall.  One  of  the  branches 
of  the  artery  may  be  constricted  through  retraction  of  the  lung  in 
interstitial  pneumonia. 

Symptoms  are  confined  in  the  main  to  the  secondary  effects 
on  the  right  ventricle  or  to  congestion  of  the  lung  back  of  the  seat 
of  stenosis  when  this  is  situated  within  the  lung  at  a  distance  from 
the  bifurcation. 

If  the  obstruction  is  in  the  nuiin  trunk  or  in  a  branch  suffi- 
ciently close  to  the  main  stem,  the  right  ventricle  undergoes  hyper- 
trophy and  perhaps  dilatation  witli  consequent  turgescence  of  the 
veins  of  the  aortic  system  and  corresimnding  feel)leness  of  the 
pulse.  It  may  even  lead  to  relative  incompetence  of  the  pulmonary 
valve  with  its  evil  consequences. 

Diagnosis  is  attended  with  great  difficulty,  and  is  likely  to  be 
inij)(»ssiblt'.  It  must  depend  upon  the  recognition  of  right-ventri- 
cle hypertrophy  for  which  no  other  cause  can  be  determined,  or 
on  this  with  a  systolic  murninr  in  tlic  ])uliiionic  area  together  with 
intensification,  instead  (if  (liiniimtion  of  tlie  second  tone,  as  is 
the  case  in  stenosis  of  the  puhiiouic  ostium.  Systolic  pulsa- 
tion in  the  situation  of  the  trunk  of  tlie  artery — i.  e.,  in  the 
second  left  intercostal  space  close  to  the  sternum — together  with 


CONGENITAL  SMALLNESS   OF  THE   ARTERIES  773 

dulness  in  tliis  area,  would  greatly  strengthen  the  other  signs  just 
mentioned  (Romberg). 

The  prognosis  is  determined  by  the  nature  and  degree  of 
secondary  disturbance.  It  is  of  necessity  more  or  less  unfavour- 
able. 

Treatment  is  entirely  symptomatic,  and,  as  in  stenosis  of  the 
aorta,  must  aim  at  maintaining  cardiac  adequacy,  since  the  cause 
cannot  be  removed. 

VII.  CONGENITAL  SMALLNESS  OF   THE   ARTERIES 

This  state  of  the  aorta  and  arterial  system  was  studied  by 
Virchow,  who  pointed  put  its  association  with  chlorosis.  Not  only 
are  the  vessels  of  small  calibre,  but  their  coats  are  thin  and  deli- 
cate, rendering  them  particularly  liable  to  rupture,  and  they  are 
abnormally  elastic.  In  extreme  cases  the  lumen  of  the  arteries 
ma}"  be  reduced  to  a  third  of  the  normal  (Romberg). 

The  heart  is  also  abnormally  small,  the  genitalia  are  likely  to 
remain  undeveloped,  and  the  individuals  are  small  and  delicate  in 
appearance.  This  is  especially  true  of  those  who  present  the  chlo- 
rosis spoken  of.  In  other  not  pronounced  cases  of  arterial  hypo- 
plasia there  may  be  nothing  in  the  appearance  and  no  lack  of  body 
development  to  suggest  its  existence. 

Symptoms  of  this  condition  as  such  cannot  be  said  to  exist. 
The  heart,  by  reason  of  its  smallness,  is  weakened  in  its  re- 
sistance, and  is  more  than  usually  liable  to  infection  (Romberg), 
and  indeed  general  vigour  and  resistance  may  be  said  to  be 
below  par.  This  is  readily  comprehensible  in  cases  character- 
ized by  chlorosis.  The  hypoplasia  is  found  more  often  among 
females  than  males. 

Fraentzel  was  of  the  opinion  that  congenital  narrowness  of  the 
arteries  predisposed  to  hypertrophy  and  dilatation  of  the  left  ven- 
tricle, and  in  support  of  his  view  cited  instances  of  the  kind  in 
young  recruits.  Romberg,  however,  thinks  the  clinical  picture 
drawn  by  Fraentzel  is  to  be  interpreted  as  the  result  of  prema- 
turely developed  arteriosclerosis.  This  is  favoured  possibly  by  the 
smallness  of  the  arterial  system ;  and  yet,  as  a  matter  of  fact,  such 
arterial  degeneration  does  not  occur  with  special  frequency  in  the 
subjects  of  arterial  hypoplasia. 

It  is  worthy  of  note  that  rupture  of  the  aorta  and  dissecting 


774  DISEASES   OF   THE   HEART 

aneurysm  are  said  to  occur  with  relatively  greater  frequency  when 
it  is  congenitally  narrow.  The  patients  are  also  said  to  bleed  more 
easily  than  normal  persons  owing  to  the  thinness  of  the  vascular 
coats. 

Diagnosis  of  arterial  hypoplasia  is  difficult  to  make  with  cer- 
tainty. It  may  be  considered  as  possibly  present  when  palpation 
of  the  large  cervical  arteries  and  percussion  of  the  heart  show  what 
seems  to  be  abnormal  smallness  of  the  same,  and  when,  in  addition, 
the  individual  is  poorly  developed,  chlorotic,  and  possesses  deform- 
ity or  an  infantile  state  of  the  genital  organs.  It  is  possible  that 
an  expert  in  the  use  of  the  fluoroscope  might  be  able  to  recognise 
that  in  a  given  case  the  heart  and  large  vessels  were  abnormally 
undersized. 

Prognosis. Congenital  narrowness  of  the  arteries  affects 

life  prospect  only  when  the  hypoplasia  is  considerable  and  is  at- 
tended with  chlorosis.  In  such  cases  there  is  danger  of  some  of  the 
consequences  that  have  already  been  considered. 

Treatment  cannot  affect  the  underlying  condition,  and  is 
therefore  limited  to  attempts  at  relieving  or  modifying  such  effects 
as  may  result. 


CHAPTER  XXXIV 
ANEURYSM  OF  THE  THORACIC  AORTA 

Aneurysms  have  been  the  object  of  interested  study  for  several 
centuries  both  to  anatomists  and  clinicians.  The  names  of  many 
celebrated  men  are  connected  with  the  history  of  this  arterial  dis- 
ease, and,  as  might  be  expected,  they  were  at  first  the  names  of 
anatomists  who  studied  the  subject  mainly  on  the  dead  body. 
Methods  of  diagnosis  were  crude  and,  very  naturally,  not  equal  to 
the  discovery  of  such  obscure  affections  as  intrathoracic  aneurysm. 
I^evertheless  it  is  worthy  of  record  that  Vesalius  made  a  diagnosis 
of  aortic  aneurysm  in  1567.  Malpighi  and  Morgagni  wrote  on 
the  subject  and  added  to  the  facts  concerning  it.  There  has  been 
scarcely  an  author  of  note  since  who  has  not  attempted  to  add  to 
our  knowledge  on  the  subject,  and  to  some  of  them  the  profession 
is  greatly  indebted.  Lancisi,  Scarpa,  Corvisart,  Hodgson,  Stokes, 
and  in  our  own  time  Eppinger  and  Thoma,  are  names  that  are  inti- 
mately linked  with  the  history  of  aneurysm. 

In  this  chapter  it  is  proposed  to  deal  exclusively  with  the  dis- 
ease as  it  affects  the  aorta  within  the  thorax,  a  condition  that  pos- 
sesses peculiar  interest  for  the  physician.  Aneurysms  of  periph- 
eral arteries  belong  to  the  province  of  the  surgeon  and  hence  are 
left  to  surgical  works  for  consideration. 

Morbid  Anatomy. — An  aneurysm  is  a  circumscribed  dilata- 
tion of  an  artery ;  and  as  such  must  be  distinguished  from  the  uni- 
form widening  of  an  artery,  which  results  from  sclerosis.  The 
three  main  divisions  that  are  made  of  aneurysms  are,  (A)  true, 
(B)  dissecting,  (C)  false.  By  false  aneurysm  is  meant  a  circum- 
scribed collection  of  blood  that  has  escaped  from  an  artery  into 
the  surrounding  tissues,  hence  a  ha?matoma.  The  walls  of  the 
tumour  are  not  composed  of  the  arterial  coats,  and  therefore,  ac- 
cording to  von  Schroetter,  it  should  not  have  the  term  aneurysm 

775 


776  DISEASES  OF  THE   HEART 

applied  to  it  at  all.  A  dissecting  aneurysm  is  one  in  which  the 
stream  of  blood  penetrates  through  a  rent  in  the  intima  into  the 
parts  beneath,  and  burrowing  its  way  either  between  the  inner  and 
middle  coats  or  in  the  layers  of  the  media,  thus  dissects  up  the 
intima  for  a  variable  distance.  In  some  instances  the  blood-current 
again  breaks  through  the  intima  and  becomes  reunited  with  the 
main  stream.  This  condition  may  be  of  long  standing  and  is 
scarcely  open  to  recognition. 

True  aneurysm  is  therefore  the  condition  in  which  are  ful- 
filled the  requirements  stated  in  the  definition.  The  two  sub- 
divisions of  this  form  of  tumour  which  best  meet  the  facts  as 
observed  by  the  clinician  are  (1)  fusiform  and  (2)  sacculated 
aneurysm.  By  the  former  is  meant  a  localized  dilatation  of  an 
artery  involving  its  entire  circumference;  while  by  sacculated  is 
meant  a  dilatation  limited  to  one  side,  and  hence  involving  but  a 
portion  of  its  circumference. 

Aneurysm  of  the  aorta  may  be  either  fusiform  or  saccular,  but 
the  latter  is  the  more  common.  All  three  coats  are  involved  in 
the  bulging  but  are  not  all  retained  in  the  wall  of  the  aneurysm. 
The  intima  extends  into  the  sac  to  a  greater  or  less  distance,  but 
is  then  lost.  The  portion  that  persists  usually  presents  the  changes 
of  arteriosclerosis,  as  does  also  the  inner  coat  of  the  aorta,  in  the 
neighbourhood  of  the  tumour. 

The  media  is  also  involved  in  the  destructive  process  which 
has  favoured  the  fornuition  of  the  aneurysm.  Its  muscular  fibres 
are  degenerated  or  wholly  lost  and  its  elastic  elements  show  signs 
of  granular  change.  In  places,  the  middle  coat  may  be  entirely 
destroyed;  and  when  such  is  the  case,  together  with  loss  of  the 
intima,  the  wall  of  the  sac  is  composed  solely  of  the  adventitia. 
This  latter  is  also  thickened  and  infiltrated  with  inflammatory 
products. 

The  pouch  which  has  thus  been  formed  communicates  with  the 
lumen  of  the  aorta  by  an  opening  of  variable  size,  but  almost  al- 
ways smaller  than  is  the  calibre  of  the  sac.  The  interior  of  the 
aneurysm  is  apt  to  be  lined  by  coagula  in  the  form  of  layers  of  a 
whitish  colour.  The  most  internal  of  tliese  lamina  is  likely  to  be 
reddish  and  soft,  while  the  more  deeply  situated  layers  are  firm 
as  well  as  white.  The  degree  of  thrombus  formation  within  the 
aneurysm  is  variable,  but  does  not  usually  fill  up  its  lumen. 


ANEURYSM  OF  THE  THORACIC  AORTA         777 

Exceptionally,  however,  when  the  sac  is  not  very  large  and  its 
opening  into  the  channel  of  the  aorta  is  small,  its  cavity  may  be 
entirely  filled  with  coagrila  so  as  to  obliterate  the  sac.  The  inner- 
most layer  of  fibrine  then  forms  a  firm  wall  nearly  on  a  level  with 
the  intima.  Its  surface  is  apt  to  be  rough  and  calcified.  Although 
an  aneurysm  may  in  this  manner  undergo  spontaneous  arrest,  still 
the  degeneration  of  the  arterial  coats  which  led  originally  to  the 
formation  of  that  aneurysm  is  likely  to  favour  the  development  of 
others,  so  that  multiple  aneurysms  are  not  at  all  uncommon. 

Aortic  aneurysms  differ  much  in  shape  and  size.  Thus  a  sac- 
culated aneurysm  may  have  other  sacs  springing  from  its  walls  so 
that  the  tumour  presents  an  irregular  outline.  In  size  the  sac  may 
vary  from  that  of  a  small  nut  all  the  way  to  that  of  a  man's 
head.  Aneurysms  may  be  situated  at  any  point  along  the  course 
of  the  aorta  from  just  above  the  ring  to  the  termination  of  the 
abdominal  portion. 

The  disastrous  effects  of  aortic  aneurysm  are  not  confined  to 
the  vessel,  but  consist  of  all  the  changes  in  structure  and  position 
of  neighbouring  organs  produced  by  pressure  of  the  sac.  The  na- 
ture and  extent  of  these  secondary  pressure  effects  are  determined 
by  the  situation  as  well  as  the  size  of  the  aneurysm.  Aneurysms 
involving  the  sinuses  of  Valsalva  are  not  apt  to  attain  much  size, 
yet  their  influence  on  the  heart  is  very  disastrous  and  they  are 
especially  liable  to  rupture  into  the  pericardium,  causing  sudden 
death. 

Aneurysms  of  the  arch  displace  the  heart  downward  (Fig.  109) 
and  it  may  be  forward  or  to  the  left,  but  they  rarely  occasion 
hypertrophy  of  the  left  ventricle  unless  the  aortic  valves  have 
been  rendered  incompetent.  The  latter  condition  is  likely  to  result 
when  the  sac  springs  from  the  ascending  or  transverse  arch  and  has 
attained  great  size.  I  recall  a  man  whom  I  treated  for  months 
for  aortic  regurgitation  without  suspecting  the  existence  of  an 
aneurysm  until  quite  suddenly  signs  of  pressure  on  the  left  lung 
arose.  Even  then  other  signs  of  the  aneurysm  were  not  at  all  dis- 
tinct, yet  were  of  such  a  kind  as  to  render  its  presence  certain. 

Other  effects  of  aortic  aneurysm  than  those  already  mentioned 
will  be  left  for  consideration  under  S;)Tnptoms. 

Etiology. — Arteriosclerosis  has  long  been  recognised  as  pre- 
disposing to  the  development  of  aneurysm.     It  is  objected  by  Ep- 


778  DISEASES  OF  THE  HEART 

pinger  that  the  changes  of  sclerosis  tend  to  render  the  vessel  more 
rather  than  less  resisting,  an  objection  that  is  also  recognised  by 
Thoma.  Consequently  the  latter  points  out  that  aneurysm  is  likely 
to  develop  during  the  time  of  primary  degeneration  and  weakness 
of  the  media,  before  compensatory  thickening  of  the  inner  coat 
has  taken  place.     This  will  be  referred  to  again. 


Fio.  109. — Skiagraph  showing  Aneurysm  of  Aokta  with  Disi'i.acemext  of  the  Heart 
Downward  and  to  tiik  Lkkt. 

Syphilis  is  an  uii(l()ul)t('(l  factor  in  tlic  causation  of  aortic 
aneurysm,  and  yet  wide  differences  exist  in  the  opinions  of  writers 
concerning  the  frequency  of  its  relation  to  this  form  of  vascular 
disease.  The  extremes  are  represented  by  M.  Schmidt,  who  finds 
syphilis  present  in  29  per  cent  of  cases,  and  Drummond,  who  be- 
lieves that  lues  is  responsible  for  aortic  aneurysm  in  every  in- 
stance— i.  e.,  100  per  cent.     My  exjierience  leads  me  to  look  upon 


ANEURYSM   OP,  THE  THORACIC   AORTA  7T9 

Drummond's  opinion  as  too  extreme,  and  to  accept  Gerhard t's  53 
per  cent  as  much  nearer  the  truth. 

Age  is  a  predisposing  factor  of  great  importance,  since  aneu- 
rysm of  the  thoracic  aorta  is  undoubtedly  more  frequent  after  than 
before  the  fortieth  year.  The  decade  of  life  in  which  it  is  most 
common  is  still  unsettled,  and  figures  differ  all  the  way  from  the 
fourth  decade  (Crisp)  to  the  seventh  (Juda,  Barsdorff).  Thoma's 
notion  is  that  persons  are  especially  liable  to  the  development  of 
aortic  aneurysm  at  or  about  the  age  of  forty,  in  consequence  of 
diminished  resistance  of  the  vascular  coats  at  this  time.  There  is, 
he  thinks,  a  period  of  about  a  year  at  this  age  when  the  weakness 
of  the  media  has  not  yet  become  offset  by  growth  of  connective 
tissue  in  the  intima,  and  during  which  time  the  coats  of  the  vessel 
are  therefore  liable  to  yield  to  excessive  blood-pressure  at  one  or 
more  points  resulting  in  future  aneurysm. 

I  have  under  observation  at  the  present  writing  a  muscular 
man  of  forty-four  who  gives  no  history  or  signs  of  previous  syphilis, 
but  who  has  been  a  more  than  usually  active,  energetic  business 
manager  in  a  line  of  work  that  necessitated  much  physical  exer- 
tion. This  patient  suffers  from  symptoms  which,  together  with 
stiff  arteries  and  suggestive  but  not  conclusive  physical  signs,  are 
yet  suspicious  of  fusiform  aneurysm  of  the  arch.  The  age  of  this 
person,  his  occupation,  and  the  state  of  his  arteries,  are  all,  from 
an  etiological  standpoint,  highly  suggestive  and  strengthen  the 
conclusion  to  be  drawn  from  the  clinical  findings. 

Sex  is  likewise  a  predisposing  element  in  the  class  of  cases 
now  under  consideration.  Men  are  without  doubt  far  more  liable 
to  aneurysm  than  are  members  of  the  gentler  sex.  Thus  of  a  total 
of  425  cases  of  aortic  aneurysm  analyzed  by  Hodgson,  Bizot,  and 
Browne,  and  cited  by  Gibson,  380  occurred  in  males  and  only  45 
in  females.  This  striking  preponderance  of  men  is  not  to  be  at- 
tributed to  any  quality  inherent  in  sex  per  se  as  inferior  vascular 
resistance  on  the  part  of  men^  but  to  the  greater  liability  of  males 
to  all  those  factors  which  favour  the  development  of  arteriosclero- 
sis as  well  as  their  greater  exposure  to  syphilis  and  conditions 
of  vascular  strain  which,  acting  in  conjunction  with  vascular 
degeneration,  are  known  to  predispose  to  the  occurrence  of 
aneurysm.  Sex  is  therefore  only  incidentally  of  etiological  in- 
fluence. 


Y80  DISEASES  OP  THE   HEART 

Two  other  factors  that  are  mentioned  as  predisposing  to  aortic 
aneurysm  are  the  abuse  of  alcohol  and  occupations  which  necessi- 
tate vascular  overstrain.  Both  are  recognised  causes  of  arterio- 
sclerosis, and  as  such  operate  in  the  production  of  aneurysm ;  but, 
in  addition,  overwork  subjects  the  aorta  to  strain  at  a  period  of  life 
when,  according  to  Thoma's  view,  the  vessel-wall  is  least  able  to 
endure  high  intravascular  pressure.  Such  influences  are  inde- 
pendent of  sex,  and  yet  are  some  of  the  things  which  render  men 
more  liable  to  aneurysm  than  are  women. 

Race,  which  is  said  to  exert  a  certain  degree,  of  influence,  can 
scarcely  be  separated  from  conditions  of  M'ork,  habits,  etc.,  to 
which  peoples  of  some  countries  are  especially  subjected.  Thus 
aoVtic  aneurysm  is  particularly  frequent  in  England.  The  English 
appear  to  be  more  than  commonly  subject  to  arterial  degeneration, 
and  this  fact,  acting  in  conjunction  with  heavy  toil  in  the  manifold 
workshops  of  their  country,  probably  accounts  for  the  relatively 
great  frequency  of  thoracic  aneurysm  among  them.  Traumatism 
cannot  be  ignored  in  the  production  of  aneurysm  of  peripheral 
arteries,  and  probably  also  of  the  abdominal  aorta,  but  it  is  diffi- 
cult to  see  how  injury  can  have  direct  etiological  relation  to  aneu- 
rysm of  that  portion  of  the  vessel  which  is  situated  deeply  within 
the  thorax  and  is  ])rotccted  by  its  bony  walls.  It  certainly  could 
only  act  in  connection  with  already  existing  degeneration  of  the 
media.  If  under  such  conditions  trauma — e.  g.,  a  fall  from  a 
height — were  to  suddenly  raise  blood-pressure,  it  might  possibly 
induce  laceration  of  the  middle  coat  and  thus  be  an  indirect  cause 
of  aneurysm. 

The  iiilhu'iK'o  r»f  malignant  endocarditis  in  the  causation  of 
so-called  mycotic  aneurysms  has  been  emphasized  by  Epi)inger  and 
is  generally  recognised.  Aneurysms  of  this  origin  are  usually  lo- 
cated in  peripheral  vessels,  and  yet  it  is  possible  for  such  aneu- 
rysm to  be  aortic,  as  shown  by  the  case  mentioned  by  Osier  as  hav- 
ing occurred  in  the  Montreal  General  TTos]utal.  In  this  case  there 
were,  in  addition  to  ulcerative  endocarditis,  four  saccular  dilata- 
tions of  the  aorta,  one  large  and  three  small  ones.  Embolism  may 
also  be  a  cause  of  aneurysm  of  the  arch  as  well  as  of  other  arteries, 
as  shown  by  reported  instances  in  which  the  lodgment  of  an  em- 
bolus on  the  intima  of  the  ascending  aorta  has  been  discovered  and 
was  associated  with  circumscribed  inflammatory  change.      Osier 


ANEURYSM  OP  THE  THORACIC  AORTA  T81 

thinks  it  possible  for  such  an  embolus,  if  consisting  of  a  calcareous 
plate,  to  lacerate  the  intima  and  thus  initiate  aneurysm. 

Lastly,  Osl^  believes  there  may  be  an  inherent  weakness  of 
the  vascular  coats  which  predisposes  individuals  to  aneurysm,  and 
cites  the  instance  of  Dr.  Thomas  King  Chambers,  who,  after  hav- 
ing had  one  of  the  left  popliteal  artery,  and  eleven  years  after- 
ward another  in  the  right  leg,  finally  developed  "  aneurysms  of 
the  carotid  arteries." 

Symptoms. — Cases  of  aortic  aneurysm  may  be  divided  into 
three  groups : 

(1)  Those  in  which  the  tumour  fails  to  declare  its  presence  by 
either  subjective  or  objective  symptoms.  Such  aneurysms  are  usu- 
ally small  and  are  only  discovered  at  the  necropsy,  when  they  may 
be  found  associated  with  some  other  clinically  recognisable  disease 
or  as  the  cause  of  unexpected  death  through  rupture.  When  the 
sac  is  situated  just  above  the  aortic  ring,  it  is  very  apt  to  rupture 
into  the  pericardium.  This  was  found  to  be  the  case  in  75  out 
of  289  cases  of  rupture  from  a  total  of  953  instances  of  aortic 
aneurysm  analyzed  by  Hare  and  Holder. 

(2)  Aneurysms  which  occasion  subjective  symptoms  as  the 
leading  feature  of  the  case.  In  the  majority  of  cases  objective  signs 
are  also  present,  but  often  of  so  indefinite  a  character  as  to  furnish 
no  clear  information  concerning  the  nature  of  the  tumour  occasion- 
ing pressure.  Such  cases  belong  to  Bramwell's  second  category. 
They  may  be  said  to  correspond  also  to  Broadbent's  subdivision  of 
cases  which  occasion  symptoms  but  not  signs  of  aneurysm. 

(3)  Aneurysms  which  produce  distinctive  physical  signs.  These 
are  generally  united  with  symptoms  of  greater  or  less  severity, 
but  the  objective  manifestations  of  the  disease  are  sufficiently  pro- 
nounced to  warrant  their  classification  in  a  separate  group. 

Aortic  aneurysms  may  also  be  classified  according  to  their 
situation — e.  g.,  of  the  ascending,  of  the  transverse,  and  of  the 
descending  portion  of  the  arch,  etc.  Indeed,  one  cannot  deal 
with  this  subject  adequately  and  clearly  without  describing  the 
features  distinctive  of  aneurysm  in  the  several  locations.  There 
are,  however,  certain  general  features  shared  to  a  greater  or  less 
extent  by  all  aneurysms,  whatever  their  position  along  the  course 
of  the  thoracic  aorta,  and  hence  these  will  be  considered  first. 

Such  symptoms  are  the  result  of  pressure,  and  hence  it  is  plain 


782  DISEASES  OF  THE  HEART 

that  variations  in  pressure  phenomena  are  determined  by  several 
factors,  as  the  size  of  the  sac  and  the  direction  in  which  it  grows, 
as  well  as  the  portion  of  the  aorta  from  wliich  it  springs.  More- 
over, aneurysms  are  liable  to  change  their  direction  of  growth,  so 
that  symptoms  sometimes  differ  in  character  and  intensity  from 
time  to  time.  Indeed  it  may  be  said  that  such  lack  of  constancy 
is  generally  regarded  as  one  of  the  points  of  distinction  in  favour 
of  vascular  as  against  solid  tumours. 

Pain  is  one  of  the  earliest  and  most  constant  symptoms  of  tho- 
racic aneurysm.  Its  nature  and  severity  depend  upon  the  direction 
in  which  the  sac  develops.  If  this  is  towards  the  surface  of  the 
chest,  or,  as  Walshe  termed  it,  "  centrifugal,"  pain  appears 
earlier,  is  more  constant,  and  more  like  what  is  called  neuralgic, 
is  sharp  and  lancinating  or  dull  and  aching,  and  is  not  infrequently 
described  as  boring,  grinding,  cutting,  burning,  etc.  As  it  is  due 
to  pressure  upon  the  intercostal  nerves  or  branches  of  the  brachial 
plexus,  it  is  apt  to  radiate  along  the  lines  of  these  nerves,  hence 
around  the  chest,  up  into  the  side  of  the  neck,  dowm  the  arm,  etc. 

As  a  rule,  the  pain  is  confined  to  nerves  connected  with  the 
first,  second,  third,  and  fourth  spinal  segments  (Head),  and  is 
associated  with  tender  areas  in  the  upper  part  of  the  thorax  at 
either  side,  but  especially  at  left  of  the  sternum.  Such  areas  of 
tenderness  are  not  characteristic  of  aortic  aneurysm,  however,  for 
they  may  be  sjanptomatic  of  various  diseases  of  the  intrathoracic 
viscera.  The  pain  of  aneurysm  is  apt  to  be  very  constant,  and  in 
this  regard  indicative  or  suggestive  of  tumour  rather  than  of  any 
other  disease  not  occasioning  pressure. 

If  the  sac  grows  inward  towards  the  more  yielding  and  less 
sensitive  structures,  it  is  not  so  apt  to  give  rise  to  such  severe  pain, 
and  hence  this  symptom  is  likely  to  be  overshadowed  by  some  other 
more  distressing  symptom,  as  dyspnoea  or  cough.  The  character  of 
the  pain,  too,  when  this  is  experienced,  is  apt  to  be  more  dull  and 
oppressive,  and  does  not  radiate  so  widely  in  tlie  wall  of  the  chest 
or  the  upi)er  extremity.  Although  the  pain  of  aneurysm  is  apt  to 
be  constant,  it  is  liable  to  paroxysmal  exacerbations  which  greatly 
increase  the  suffering.  Pain  is  also  apt  to  be  influenced  somewhat 
by  the  position  of  the  patient's  body.  For  example,  it  is  apt  to 
be  intensified  when  the  patient  lies  in  such  a  manner  as  to  permit 
the  sac  to  gravitate  or  press  more  strongly  upon  the  irritated  and 


ANEURYSM  OP  THE  THORACIC  AORTA         T83 

painful  nerve.  Per  contra,  suffering  is  lessened  by  attitudes  which 
allow  the  sac  to  fall  away  from  the  part  previously  pressed  upon. 
Such  postural  variations  in  the  pain  arc  not  often  marked,  but  are 
seen  sufficiently  often  to  merit  attention. 

It  is  stated  also  that  in  some  cases  the  pain  is  what  is  known 
as  intrinsic,  by  which  is  meant  pain  experienced  in  the  sac  itself 
or  in  the  aorta  either  from  acute  aortitis  or  from  internal  pressure. 
Pain  of  this  origin  is  evoked  or  aggravated  by  increase  of  blood- 
pressure,  and  is  dull  or  aching  in  character  and  substernal  in  loca- 
tion. It  is  likely  to  be  lessened  whenever  vascular  tension  is  low- 
ered. Extrinsic  pain  or  that  due  to  pressure  may  disappear  after 
the  structure  subjected  to  pressure  has  been  destroyed — e.  g.,  after 
the  bony  wall  has  been  eroded  and  the  tumour  is  permitted  to  grow 
without  the  restraint  of  rigid  structures.  I  recall  the  instance  of 
an  enormous  aneurysm  which  had  thus  penetrated  the  chest-wall 
and  was  covered  only  by  a  thin  layer  of  skin,  and  in  which  case 
the  man  made  no  complaint  of  pain  whatever. 

Dyspnoea  is  another  very  common  symptom  of  aortic  aneurysm, 
but  varies  much  in  severity.  It  is  of  course  most  pronounced  when 
the  growth  of  the  tumour  is  inward  and  pressure  is  exerted  on  the 
trachea,  large  bronchi,  or  lungs.  Very  distressing  paroxysms  of 
dyspnoea  are  occasioned  by  irritation,  not  paralysis,  of  one  of  the 
recurrent  laryngeal  nerves,  more  often  the  left,  and  are  due  to 
laryngeal  spasm.  There  is  apt  to  be  an  associated  feeling  of  con- 
striction and  perhaps  pain  in  the  side  of  the  throat.  In  a  case  of 
the  kind  coming  under  my  observation,  the  man  felt  the  painful 
sense  of  constriction  in  the  side  of  the  neck  corresponding  with  the 
recurrent  nerve  affected,  and  described  the  sensation  as  beginning 
in  the  left  side  of  the  larynx  and  running  thence  along  the  side 
to  the  back  of  the  neck. 

I  have  quite  recently  seen,  in  consultation  with  Dr.  Grorgas,  a 
man  of  fifty  with  aneurysm  of  the  ascending  and  transverse  arch 
whose  dyspnoea  was  extreme,  and  compelled  him  to  maintain  the 
right  lateral  decubitus.  Change  of  position  induced  a  paroxysm 
of  air-hunger  accompanied  by  uncontrollable  coughing.  It  was 
impossible  for  him  to  rest  on  the  left  side,  or  indeed  to  lie  back 
against  the  pillows.  In  this  respect  his  dyspnoea  corresponded 
with  what  appears  to  be  a  quite  common  experience — i.  e.,  the 
influence  of  posture  over  the  intensity  of  the  dyspnoea  and  of 


784  DISEASES  OF  THE   HEART 

change  of  position  in  evoking  a  paroxysm  of  respiratory  difficulty 
that  is  very  like  an  asthmatic  attack.  The  subsequent  history  of 
this  case  is  interesting  and  instructive.  Having  received  a  hope- 
less prognosis  from  his  medical  advisers,  he  resorted  to  a  Christian 
Science  healer.  Owing  to  a  coincident  change  in  direction  of 
pressure,  his  sufferings  abated  and  he  again  got  about,  the  im- 
provement being  attributed  by  himself  and  family  to  this  treat- 
ment. After  a  respite  from  suffering  of  several  weeks,  his  former 
symptoms  recurred  with  aggravated  intensity  and  shortly  there- 
after the  man  died. 

Dr.  Gorgas  made  an  autopsy  and  discovered  an  enormous  sac 
that  had  not  only  produced  pressure  on  the  right  lung  and  sur- 
rounding structures,  but  had  caused  the  erosion  of  several  dorsal 
vertebra?. 

Difficulty  of  breathing  is  very  apt  to  be  accompanied  by  stridor, 
which  may  be  so  intense  as  to  be  audible  at  a  distance  and  occasion 
pronounced  fremitus.  This  stridulous  respiration  is  due  to  con- 
striction of  the  trachea  or  of  a  bronchus  and  consequent  interference 
with  the  expulsion  of  mucus  accumulated  behind  the  point  of  com- 
pression. 

Cough  is  a  very  common  symptom  in  cases  of  thoracic  aneu- 
rysm, but  is  variable  in  both  frequency  and  severity.  In  some  cases 
it  is  so  distressing  as  to  rob  the  patient  of  needful  rest,  and  when 
once  excited  is  so  prolonged  and  intractable  as  to  necessitate  abso- 
lute repose  in  a  given  position  pud  even  require  the  free  use  of 
morphine.  When  due  to  pressure  upon  the  trachea,  as  occurs  most 
fr('(|uently  in  cases  of  aneurysm  of  the  transverse  arch,  the  cough 
is  a])t  to  possess  a  harsh  strident  character;  that  by  Wyllie  was 
likened  to  the  note  of  a  gander,  and  hence  is  known  as  the  "  goose 
cough."  In  some  instances  it  may  be  of  a  toneless,  muffled  charac- 
ter, probably  in  consequence  of  paralysis  of  a  vocal  chord.  The 
causes  of  cough  are  various,  as  (A)  reflex  irritation  from  pressure 
on  the  vagus  or  recurrent  laryngeal  nerve,  (B)  compression  of 
trachea  or  bronchus,  (C)  direct  impingement  on  the  lung  with  re- 
sulting retention  of  secretions  or  with  an  actively  destructive 
process, 

Expecioraiion  is  apt  to  be  associated  with  cough,  and  may  con- 
sist of  mucus  and  serum,  muco-pus,  and  in  cases  of  ])ulmonary  gan- 
grene, of  offensive  material  characteristic  of  this  affection. 


AI^EURYSM  OF  THE  THORACIC  AORTA  785 

Hcemoptysis  is  by  no  means  uncommon  in  cases  of  aortic  aneu- 
rysm, in  Avhich  event  the  blood  may  come  from  granulations  situ- 
ated on  the  tracheal  mucosa  (Osier),  from  bronchial  congestion, 
or  from  destruction  of  a  lung,  or  from  the  sac  itself,  what  is  then 
known  as  weeping  of  the  aneurysm.  Such  hsemoptyses  may  occur 
from  time  to  time  over  a  protracted  period,  even  for  months. 

I  vividly  recall  the  instance  of  a  man  with  unmistakable  aneu- 
rysm of  the  upper  portion  of  the  descending  aorta,  whose  clinical 
picture  was  that  of  phthisis.  The  tumour  occasioned  destructive 
pressure  on  the  left  lung,  with  pronounced  dulness,  bronchial  res- 
piration, and  a  multitude  of  coarse  and  fine  bubbling  rales,  fre- 
quent harassing  cough,  and  copious  purulent  sputum  which  was 
occasionally  streaked  with  blood.  In  another  case  of  aneurysm 
similarly  situated,  pressure  was  chiefly  exerted  upon  the  left  bron- 
chus with  consequent  dyspnoea,  cough,  and  copious  rales  due  to 
retention,  since  there  w^as  very  little  expectoration. 

Dysphagia  is  another  very  frequent  subjective  symptom,  which 
is  occasioned  by  aneurysms  of  the  transverse  and  descending  por- 
tions of  the  arch,  or  when  a  sac  situated  on  the  descending  aorta 
exerts  pressure  upon  the  oesophagus.  The  patient  not  infrequently 
speaks  of  the  ingesta  seeming  to  stick  at  a  certain  point  in  their 
passage  downward.  If  the  aneurysm  is  situated  low  down  near 
the  diaphragm  it  may  cause  regurgitation  of  the  food.  Digestive 
disorders,  properly  speaking,  do  not  form  a  part  of  the  clinical 
history  of  thoracic  aneurysms.  They  may  be  present  nevertheless, 
and  are  then  the  result,  in  part  at  least,  of  the  stasis  within  the 
portal  system  and  its  tributaries  occasioned  by  pressure  on  the 
great  veins  in  the  thorax. 

All  aneurysms  of  the  arch  do  not  occasion  appreciable  inter- 
ference with  the  flow  of  blood  out  of  the  venous  system.  When, 
however,  an  aneurysm  attains  considerable  size  it  can  scarcely  fail 
to  affect  circulation  by  mechanical  pressure.  One  or  both  of 
the  vense  cavee  may  be  compressed,  and  to  such  a  degree  that  the 
circulation  can  only  be  carried  on  by  means  of  collateral  vessels. 

Such  a  condition  is  admirably  shown  in  Fig.  110,  which  is  taken 
from  a  photograph  kindly  furnished  me  by  Dr.  Emil  Beck.  This 
man,  aged  thirty-seven,  was  first  seen  by  Dr.  Beck  in  October  of 
1901,  at  which  time  his  complaint  was  of  cough,  dyspnoea  and  in- 
ability to  lie  down.  He  gave  a  history  of  syphilis  sixteen  years 
50* 


786 


DISEASES   OF   THE   HEART 


FlO.  no. — DiLATATInx    OF    SUPERFICIAL  VeINS    SeCONHAHY   Ti)    PuESSUUE    BY    ANEURYSM   ON 

Ven^  Cav^. 


before,  for  which  he  received  very  inadequate  treatment.  His  occu- 
pation was  that  of  a  metal-polisher,  which  necessitates  the  putting 
forth   of  considerable,  strength  in  pressing  the  metal  against  a 


ANEURYSM   OF  THE  THORACIC  AORTA  78Y 

polishing  wheel.     Here,  then,  were  two  factors  both  operative  in 
the  etiology  of  aneurysm. 

His  one  initial  symptom  of  breathlessness  on  exertion  devel- 
oped slowly,  and  did  not  necessitate  abandonment  of  work  and  the 
sport  of  playing  baseball  until  nearly  a  year  after  it  was  first 
noticed.  When  Dr.  Beck  examined  the  patient  there  was  a  per- 
ceptible fulness  of  the  neck  and  bulging  in  the  aortic  area.  This 
tumour  pulsated  and  gave  a  systolic  bruit.  The  pulses  of  the  right 
half  of  the  neck  and  of  the  corresponding  arm  were  distinctly 
smaller  than  their  fellows  on  the  left  side.  The  diagnosis  was 
accordingly  made  of  aneurysm  of  the  ascending  and  transverse 
aorta. 

Cyanosis  and  turgescent  veins  were  marked.  He  was  then  ad- 
vised to  enter  St.  Joseph's  Hospital,  in  the  service  of  Dr.  Carl 
Beck,  for  the  purpose  of  treatment.  Rest  and  iodide  of  potash  did 
not  seem  to  ameliorate  his  condition,  and  he  left  the  hospital. 

An  aggravation  of  symptoms  and  evident  increase  in  the  size 
of  the  sac  led  the  patient  to  re-enter,  in  January,  1902,  when  he 
was  given  hypodermic  injections  of  gelatin  (2  per  cent  in  30 
cubic  centimetres  of  normal  salt  solution)  which  were  administered 
once  a  w^eek,  subsequently  increased  to  45  cubic  centimetres,  until 
he  had  received  ten  such  injections  in  all. 

Under  this  treatment  pressure  symptoms  nearly  disappeared, 
and  the  patient  felt  so  well  that  he  again  left  the  hospital.  Through 
the  courtesy  of  Dr.  E.  Beck,  I  had  the  opportunity  of  examining 
him  a  number  of  weeks  later.  The  distention  of  the  superficial 
veins  was  then  as  shown  in  Fig.  110,  while,  viewed  from  the  side, 
there  w^as  the  evident  bulging  of  the  chest  shown  in  Fig.  111.  The 
arteries  of  the  right  arm  and  corresponding  half  of  the  neck  were 
manifestly  less  filled  than  those  on  the  opposite  side.  There  was 
a  feeble  pulsation  in  the  prominent  area,  and  tracheal  tugging  could 
be  plainly  felt. 

Percussion  elicited  an  area  of  flatness  having  a  semicircular 
outline  below  and  extending  from  beneath  the  middle  of  one  clavi- 
cle across  the  upper  sternal  region  to  about  the  same  distance  on 
the  other  side.  This  area  is  shown  by  a  shaded  area  in  Fig.  112. 
Over  this  area  could  be  heard  a  dull  first  tone  accompanied  by  a 
systolic  bruit  and  succeeded  by  a  loud,  ringing  second  sound. 

The  area  of  relative  cardie  dulness  is  also  shown  in  Fig.  112, 


788 


DISEASES  OF  THE   HEART 


Fi<i.  111.— J'lioToouAiMi    OF    Cask    ok    Aortk-    Ani-.ury.sm,  siiowino    8i.i..iit    IJi  i.uino   of 

Anterior  Chest  Wall. 


and  from  its  position  indicates  displacement  of  the  heart  down- 
ward and  to  the  left.  Its  sounds  were  clear,  but  the  aortic  second 
was  very  loud  and  motallic. 


ANEURYSM  OF  ^HE  THORACIC  AORTA 


789 


The  liver,  as  indicated  by  the  outline  at  the  bottom  of  the 
figure,  was  evidently  engorged  as  well  as-  probably  somewhat  de- 
pressed, being  palpable  and  having  an  area  of  greatly  increased 
flatness. 

The  man  admitted  having  previously  noticed  some  difficulty  in 
swallowing.  He  had  not  experienced  pain  to  any  extent,  but  in 
the  last  two  weeks  had  begun  to  notice  some  dull  pain  in  the  front 
of  the  chest  at  right  of  the  sternum.  This,  it  seemed  to  me,  indi- 
cated an  increase  of  pressure 
upon  the  parietes,  the  sac  hav- 
ing changed  its  direction  of 
growth,  and  hence  its  pressure, 
in  the  weeks  following  his 
abandonment,  of  the  gelatin 
injections.  It  may  be  stated 
in  addition  that  the  nature  of 
this  case  was  confirmed  by  an 
X-ray  examination. 

The  interference  with  ve- 
nous circulation  in  these  cases 
may  not  only  be  declared  by 
turgescence  of  superficial  ves- 
sels, but  by  general  or  local- 
ized oedema.  Thus  the  neck 
and  upper  extremities  may  be- 
come dropsical,  or  the  oedema  may  be  limited  to  one  arm  and 
a  portion  of  the  thoracic  wall.  Inequality  of  the  pulses  on 
the  two  sides  is  very  common,  owing  to  partial  obliteration,  dis- 
placement, or  twisting  of  the  great  branches  given  off  from  the 
arch.  Displacements  of  the  heart  occur  and  the  function  of  the 
valves,  especially  the  aortic,  is  quite  likely  to  be  seriously  inter- 
fered with.  Pressure  effects  in  detail  will  be  considered  in  con- 
nection with  the  description  of  aneurysms  in  the  various  situations. 
(1)  Aneurysms  of  the  ascending  portion  of  the  arch. — These 
may  be  situated  close  to  the  aortic  ring  and  involve  the  sinuses  of 
Valsalva,  or  they  may  spring  from  the  convex  or  concave  surface. 
In  the  first  situation  they  are  apt  to  be  small  and  to  escape  detec- 
tion, first  declaring  their  presence  by  rupture  into  the  pericardium 
and  death. 


Fig.  112. — Shows  Dulness  and  Liver  Out- 
line IN  Case  of  Aneurysm  (p.  785),- 


790 


DISEASES  OF  THE  HEART 


If  the  sac  arises  from  the  convex  aspect,  it  is  likely  to  attain 
great  size  and  exert  very  obvious  pressure  effects.  If  its  direction 
of  growth  is  forward  as  well  as  lateral,  it  produces  a  pulsating 
tumour  in  the  second  and  third  interspaces  at  the  right  of  the 
sternum,  and  not  infrequently  leads  to  erosion  of  the  bony  cover- 
ing. Aneurysms  in  this  situation  may  attain  truly  enormous  di- 
mensions, and  projecting  Avith  only  the  integument  for  a  covering, 


^ 


I 


\ 


Fios.  113,  114. — Showing  Exteunal  Tumour  in  Case  of  Aoitric  Aneurysm 
(see  Figr.  115). 

necessitate  the  wearing  of  a  metal  shield,  lest  the  tumour  be  acci- 
dentally struck  and  caused  to  burst.  Figs.  11 3-11 T)  show  an 
aneurysm  in  this  location  which  had  an  external  diameter  of 
several  inches.  T  vividly  recall  another  man  sent  to  me  by  Dr.  G. 
Frank  Lydston,  who  ])r('s('iite(l  a  ])ulsating  prominence  which  oc- 
cupied the  entire  praccordia,  extending  from  one  nipple  to  the 
other,  and  from  the  upper  border  of  the  second  rib  to  the  inferior 


^ 


Fig.  115. — Post-Moetem  Specimen  of  Heart  and  Aneurysmal  Sac  from  Case  figured 

IN  Figs.  113  and  114. 


791 


Y92  DISEASES   OP  THE   HEART 

extremity  of  the  sterimm.  As  nearly  as  could  be  determined  by 
measurement  with  calipers,  the  tumour  projected  4  inches  at  its 
highest  point  above  the  level  of  the  surrounding  chest,  and  its 
diameter  was  7X8  inches.  In  places  the  enveloping  skin  was  so 
thin  and  blue  that  it  seemed  on  the  verge  of  rupture,  and  made 
me  actually  shudder  to  touch  it.  I  dared  not  place  a  stethoscope 
upon  it  firmly  enough  to  auscultate  with  accuracy,  but  so  far  as 
could  be  ascertained  the  dull,  distant  sounds  were  not  accompanied 
by  murmurs.  Where  the  heart  was  I  could  not  determine.  How 
this  man  had  been  able  to  thread  his  way  through  our  crowded 
streets  without  receiving  a  fatal  blow  on  this  thin-walled  sac  I  do 
not  know.  He  was  advised  to  protect  it  by  wearing  strapped  to 
his  chest  a  framework  or  cage  of  woven  wire.  He  was  seen  by  me 
but  twice,  and  it  is  probable  that  death  from  external  rupture  took 
place  not  long  thereafter. 

Aneurysms  in  this  situation  may  encroach  upon  the  pleural 
cavity  and  lung,  as  witness  an  instance  seen  in  the  Cook  County 
Poor-IIouse  in  which  the  necropsy  revealed  a  sac  of  enormous  size 
that  nearly  filled  the  entire  right  half  of  the  thorax  and  had  caused 
collapse  of  the  lung,  the  same  as  would  a  massive  pleuritic  exudate. 
The  side  was  motionless  and  moderately  enlarged  during  life,  flat 
and  intensely  resisting  on  percussion,  with  complete  absence  of 
cardiac  tones  and  murmurs.  Breath-sounds  were  heard  feebly  at 
the  summit  of  the  chest  behind,  close  to  the  spinal  column,  all  of 
which  fi.ndings,  together  with  distention  of  the  superficial  veins, 
were  held  to  indicate  pressure  by  a  solid  tumour  rather  than  aneu- 
rysm. 

Aneurysms  of  the  convex  portion  of  the  ascending  aorta  are 
likely  to  impinge  upon  the  superior  vena  cava  and  have  been 
known  to  rupture  into  this  vessel.  They  may  press  also  upon  the 
right  subclavian  vein  and  occasion  passive  congestion  of  the  arm 
and  other  parts  drained  by  this  vein.  In  some  instances  the  right 
recurrent  laryngeal  nerve  is  subjected  to  pressure,  with  consequent 
paresis  of  the  right  vocal  cord.  The  heart  is  also  likely  to  be 
crowded  downward  and  to  the  left,  while  the  aortic  valve  is  apt 
to  be  rendered  relatively  incompetent.  The  hypertrophy  of  the 
left  ventricle  in  such  cases  is  the  result  of  the  regurgitation  rather 
than  of  the  aneurysm  per  se. 

Aneurysms  springing  from  the  concave  portion  of  the  ascend- 


ANEURYSM  OF  THE  THORACIC  AORTA         793 

ing  aorta  may,  according  to  Osier,  occasionally  give  rise-  to  a 
tumour  at  the  left  of  tlie  sternum  and  then  occasion  great  displace- 
ment of  the  heart.  There  is  at  the  present  time  in  Ward  10  of 
Cook  County  Hospital  a  man  who  presents  such  a  tumour.  It  lies 
in  the  situation  normally  occupied  by  the  body  of  the  heart^i.  e., 
between  the  second  and  sixth  costal  cartilages,  the  left  border  of 
the  sternum,  and  1  inch  outside  of  mamillary  line — has  a  slowly 
heaving  expansile  pulsation  and  gives  forth  a  distinct,  harsh  double 
bruit  that  has  replaced  the  normal  cardiac  sounds.  The  heart,  as 
shown  by  percussion  and  the  location  of  what  appears  to  be  the 
apex-beat  in  the  seventh  interspace  midaxillary  line,  is  greatly 
displaced  downward  and  to  the  left.  Its  tones  are  rather  feebly 
audible  in  this  situation  and  are  accompanied  by  the  same  to-and- 
fro  murmur,  though  less  distinctly  than  on  the  body  of  the  tumour. 
Vascular  signs  of  aortic  regurgitation  are  present,  and  there  is  an 
indefinite  tracheal  tug.  There  are  no  signs  of  pressure  on  the  left 
recurrent  laryngeal  nerve,  and  pressure  effects  on  veins  are  not 
present.  Without  wishing  to  affirm  that  this  sac  arises  from  the 
concave  aspect  of  the  ascending  aorta,  I  yet  incline  to  the  opinion 
that  such  is  the  location,  since  the  incompetence  of  the  aortic  valve 
is  not  so  likely  in  cases  of  aneurysm  developed  from  the  descending 
portion  of  the  arch,  and  were  the  transverse  arch  the  portion 
affected,  the  tumour  would  be  likely  to  have  a  different  location. 
This  patient  has  been  an  inmate  of  the  hospital  at  various  times 
for  the  past  four  years.  Occasional  dull  pain  over  the  seat  of  the 
growth  and  dyspnoea  of  effort  are  the  only  symptoms  of  which  he 
complains. 

(2)  Aneurysms  of  the  transverse  arch,  in  the  same  manner  as 
those  just  considered,  produce  a  variety  of  effects  according  to  their 
size  and  direction  of  growth.  They  most  frequently  develop  in  a 
backward  direction,  and  then,  when  even  of  small  size,  occasion 
pronounced  symptoms  in  consequence  of  j)ressure  on  the  trachea 
and  oesophagus,  interfering  with  respiration  and  deglutition. 
Paroxysmal  cough  is  a  very  common  symptom  and  insiDiration  is 
attended  with  stridor. 

Growth  of  the  sac  forward  produces  a  tumour  at  the  upper  part 
of  the  sternum  and  to  the  right,  with  absorption  of  the  bony  struc- 
tures.    The  tumour  may  occasionally  present  at  the  left  of  the 
breastbone,  but  does  so  so  much  less  commonly  than  at  the  right  of 
51 


Y94  DISEASES  OP  THE   HEART 

the  median  line  that,  according  to  Osier,  O.  A.  Browne  found  it  but 
4  times  out  of  35  cases  of  aneurysm  of  the  transverse  arch.  These 
tumours  sometimes  reach  enormous  size  and  fill  up  the  superior 
mediastinum  so  that  they  spread  out  into  both  pleural  cavities. 

Pressure  of  these  aneurysms  is  exerted  on  the  left  recurrent 
laryngeal  nerve  and  left  bronchus,  producing  such  characteristic 
phenomena  that  these  cases  have  been  described  by  Dieulafoy  as 
Aneurysms  of  the  liecurrent  Type.  In  this  class  of  cases  symp- 
toms vary  according  to  whether  the  nerve  is  paralyzed  or  merely 
irritated  by  pressure  of  the  growth.  Paralysis  of  the  recurrent 
nerve  is  shown  by  paralysis  of  the  corresponding  vocal  cord,  which, 
examined  laryngoscopically,  is  seen  in  a  state  of  cadaveric  rigidity. 

When  the  nerve  is  merely  irritated  laryngeal  spasm  is  evoked, 
shown  by  paroxysmal  dyspncea,  lasting  from  a  few  minutes  to  sev- 
eral hours,  and  causing  very  great  distress.  There  is  also  apt  to 
be  painful  deglutition,  and  there  may  be  attacks  of  angina  pectoris 
from  pressure  on  the  cardiac  branches  of  the  recurrent  (Preble). 
Pain  in  swallowing  is  due  to  spasm  of  the  muscles  of  deglutition 
in  the  pharynx  and  gullet.  Variations  in  the  quality  and  power 
of  the  voice  are  observed  in  these  cases,  and  the  left  vocal  cord 
may  be  paralyzed  for  a  transient  period. 

Mr.  M.,  a  school-teacher,  aged  thirty-two,  was  referred  to  me  by 
Dr.  Bayard  Holmes  because  of  paroxysms  of  dyspnooa  that  were 
thought  by  the  patient  to  be  attacks  of  asthma.  The  history  was, 
that  a  year  earlier  ho  had,  one  evening,  without  previous  warning, 
been  seized  with  a  fit  of  coughing  that  was  immediately  succeeded 
by  difficulty  of  breathing  lasting  the  greater  part  of  an  hour.  As 
he  had  become  chilled  the  night  before  on  the  deck  of  a  steamboat, 
he  had  attributed  his  attack  to  having  taken  cold  and  tliouglit  no 
more  about  it. 

That  was  not  liis  last  attack,  however,  but  during  the  next  few 
months  he  experienced  several  recurrences.  During  the  six  months 
last  past  his  attacks  had  increased  in  frequency  and  intensity. 
They  came  on  at  any  time,  but  more  often  in  the  early  morning, 
waking  liim  out  of  sleep,  and  lasting  from  twenty  minutes  to  half 
an  hour.  They  were  accompanied  by  loud  wheezing  in  the  throat 
or  upper  part  of  the  chest  and  gave  him  the  sensation  of  being 
strangled.  When  tlie  attacks  subsided  he  felt  as  well  as  ever.  In 
other  respects  ho  fell:  in  good  liealth. 


ANEURYSM   OF   THE  THORACIC   AORTA  Y95 

It  was  apparent  that  this  was  not  the  clinical  history  of  bron- 
chial asthma,  but  was  highly  suggestive  of  some  organic  disease, 
especially  of  intermittent  ])ressurc.  I  therefore  inquired  concern- 
ing syphilitic  infection  and  learned  that  he  had  had  a  chancre 
twelve  years  before.  This  fact  in  connection  with  his  symptoms 
suggested  thoracic  aneurysm  as  the  possible  cause  of  pressure  on 
the  recurrent  laryngeal,  and  led  to  minute  inquiry  regarding  pain 
and  cough.  With  exception  of  a  trifling  dry  cough  to  which  he 
paid  no  attention,  he  declared  he  was  free  from  all  symptoms  ex- 
cept the  spasmodic  dyspnoea  already  described. 

The  results  of  examination  may  be  briefly  stated  as  follows: 
The  left  radial  and  carotid  pulses  seemed  not  quite  so  full  and 
strong  as  the  right,  but  the  difference  was  so  trifling  that  I  hesi- 
tated to  accredit  my  senses  lest  I  might  be  deceived  by  my  sus- 
picion of  aneurysm  into  recognising  an  asymmetry  that  did  not 
actually  exist.  Likewise  I  was  not  able  to  positively  identify  any 
abnormal  finding  in  the  investigation  of  the  heart  and  cervical 
vessels,  but  I  thought  I  recognised  a  slight  difference  in  the  in- 
tensity of  the  second  tone  on  the  two  sides  of  the  neck,  that  above 
the  left  clavicle  being  somewhat  louder  and  more  ringing  than  at 
the  right.  There  was  certainly  no  abnormal  pulsation  or  inequal- 
ity in  the  vessels  to  the  palpating  finger.  The  heart  appeared  in 
its  normal  position. 

Upon  examination  of  the  lungs,  however,  certain  abnormalities 
were  at  once  detected.  Over  the  upper  portion  of  the  chest  there 
was  a  single  inspiratory  sibilus  with  each  act,  the  rale  seeming  to 
be  more  pronounced  on  the  left.  But  the  change  that  was  most 
noteworthy  was  dulness  of  the  left  apex  above  the  clavicle  and 
in  the  first  interspace  close  to  the  left  edge  of  the  sternum.  This 
impairment  of  resonance  was  not  intense  and  yet  was  distinct. 
Over  this  area  the  breath-sounds  were  obscured  by  subcrepitant 
rales.  After  several  forced  inspirations  the  dulness  became  less 
pronounced  and  the  rales  partially  disappeared. 

These  findings  convinced  me  that  the  loss  of  resonance  was  due 
to  atelectasis,  and  that  from  the  history  of  spasmodic  dyspncea  the 
collapse  of  this  portion  of  the  left  upper  lobe  was  probably  caused 
by  pressure.  From  the  history  of  syphilis  twelve  years  before  and 
from  the  absence  of  positive  signs  on  the  part  of  the  circulatory 
apparatus,  I  was  led  to  make  an  inferential  diagnosis  of  aneurysm 


796  DISEASES  OF  THE   HEART 

of  the  traiisverso  portion  of  tli(>  iircli  and  consequent  irritation  of 
tlie  left  recurrent  laryngeal  nerve. 

Laryngoscoi)ic  examination  was  next  made,  and  aside  from 
slight  congestion  of  the  left  arytenoid  cartilage  was  negative.  The 
patient  was  then  submitted  to  an  X-ray  examination  with  the  re- 
sult that  the  fluoroscopic  screen  revealed  a  pulsating  tumour  be- 
hind the  left  edge  of  the  sternum,  while  a  skiagraph  showed  a 
distinct  though  small  shadow  in  the  same  situation. 

The  diagnosis  was  thus  confirmed  and  the  case  was  shown  to  be 
one  of  the  type  just  described.  It  is  interesting,  furthermore,  in 
two  resjoects:  first,  on  account  of  the  early  age  (thirty-two  years) 
at  which  thoracic  aneurysm  has  developed,  and  second,  because  it 
was  tlie  i)eeuliar  character  of  the  dyspnoeic  attacks  which  sug- 
gested the  possibility  of  the  disease. 

The  attacks,  which  in  this  case  were  considered  asthmatic  by 
the  patient,  were  in  reality  due  to  laryngeal  spasm ;  and  could  the 
larnyx  have  becii  inspected  during  an  attack,  the  arytenoid  carti- 
lages M'ould  probably  have  been  found  approximated  and  the  left 
vocal  cord  occupying  the  median  line.  As  a  matter  of  fact,  an  at- 
tempt to  inspect  the  larynx  during  a  spasm  was  made,  but  the 
attack  was  passing  off  and  the  laryngoscopic  examination  was 
negative. 

It  is  further  worthy  of  note,  that  paroxysmal  dysphagia  was 
not  experienced  and  that  pain  was  never  complained  of  by  this 
man.  This  accords  with  the  fact  that  dyspnoea  and  dysphagia  arc 
not  necessarily  associated  in  all  cases. 

Pressure  on  the  left  bronchus  is  another  effect  of  aneurysms 
of  the  transverse  arch  of  the  type  now  considered.  If  the  t\d)e  is 
but  slightly  constricted,  the  lung  becomes  retracted  only  sufficiently 
to  occasion  immobility  of  the  side,  tympanitic  resonance  and  di- 
minished respiratory  sounds.  When  the  bronchus  is  greatly  nar- 
rowed the  side  becomes  perceptibly  snuiller  than  its  fellow,  the 
percussion  note  is  dull,  and  respiratory  sounds  are  abolished. 
There  may  be  retention  of  the  secretions  with  rales,  bronchorrhoca, 
:ind  bronchiectasis — symptoms  which,  in  the  Montreal  General 
lIos])ital,  are  characterized  as  "aneurysmal  phthisis"  (Osier). 

Aneurysms  of  this  portion  of  the  arch  sometimes  occasion  pres- 
sure on  the  thoracic  duct.  If  they  develop  in  such  a  direction  as 
to  involve  the  innominate  or  carotid  artery,  the  condition  is  apt 


ANEURYSM  OP  THE  THORACIC  AORTA 


797 


to  be  shown  by  a  symmetry  or  delay  of  the  pulses  on  that  side. 
Pressure  on  the  sympathetic  is  another  manifestation  of  tumours 
in  this  situation,  and  is  shown  by  dilatation  and  immobility  of  the 


Fig.  116. — Trachea  from  Case  of  Euptuked  Aneurysm,  showing  Point  of  Rupture. 

pupil  when  the  nerve  is  irritated,  and  by  contraction  when  the 
sympathetic  is  paralyzed.  Tracheal  tugging  is  another  result  of 
aneurysm  of  the  transverse  arch,  as  was  first  shown  by  Oliver.     Tt 


798 


DISEASES   OF   THE   HEART 


is  due  to  the  downward  traction  of  the  sac  on  the  trachea  at  its 
bifurcation.  This  si^n  will  be  spoken  of  ai;ain  at  greater  length 
under  Palpation.  Aneurysms  in  this  situation  nia}'  rupture  into 
the  trachea  (Figs.  11(>,  117). 

(3)  Aneurysms  of  the  descending  portion   of  fhe  arch  grow 
laterally  and  posteriorly  in  the  majority  of  instances,  and  yet  it  is 


Fi(i.  117. — Oi'i>o9iTE    Side   of   Specimen   shown   in    Fig.  11)!.     Snows   Interior   of  Sac. 
Pkoke  in  Opening  into  Trachea. 


stated  that  a  tumour  of  this  portion  of  the  vessel  may  present  at 
the  left  of  the  sternum  (Sansom,  Walshe).  Phthisical  symptoms 
are  the  result  of  pressui'c  on  tlic  left  lung  or  bronchus,  dysphagia  of 
(compression  of  th(\ii'nll('t,  jiaiii  fiiuii  ei'osion  of  the  dorsal  vertebra3 


ANEURYSM  OF  THE  THORACIC  AORTA  T99 

(third  to  sixth),  and  a  tumour  in  this  situation  may  be  the  result 
of  backward  pressure.  Compression  of  the  spinal  cord  may  oc- 
casion characteristic  effects — e.  g.,  paraplegia. 

(4)  Aneurysms  of  the  descending  thoracic  aorta  are  usually 
located  low  down  near  the  diaphragm  and  produce  oftentimes  very 
obscure  symptoms.  In  an  instance  of  the  kind  which  I  saw  with  Dr. 
Bayard  Holmes,  and  which  was  not  recognised  as  aneurysm,  the 
only  complaint  was  dull  pain  vaguely  felt  in  the  lower  zone  of  the 
thorax  and  upper  abdominal  region.  The  only  thing  that  could 
be  discovered  on  examination  was  an  area  of  impaired  resonance 
and  feeble  broncho-vesicular  breath-sounds  in  the  left  infrascapu- 
lar  region,  close  to  tlie  spinal  column.  From  the  history  of  previous 
illness,  that  seemed  to  have  been  pleuritic,  and  from  the  physical 
findings,  this  area  was  erroneously  thought  to  indicate  old  adhe- 
sions. The  autopsy,  months  subsequently,  revealed  a  sac  filled  with 
dense  coagula  pressing  on  the  base  of  the  left  lung  just  above  the 
diajDhragm. 

Aneurysms  in  this  situation  may,  as  previously  stated,  cause 
dysphagia  and  regurgitation  of  solid  ingesta,  but  they  rarely  occa- 
sion respiratory  embarrassment.  Aside  from  deep-seated  pain 
they  are  not  likely  to  produce  subjective  symptoms,  and  unless,  by 
reason  of  their  size,  thev  ffive  rise  to  lateral  dulness  and  other 
signs  of  pressure  on  the  lung,  they  are  likely  to  escape  recognition. 

It  should  be  borne  in  mind  that  an  aneurysm  which  in  the 
beginning  is  confined  to  one  portion  of  the  arch  may  as  time  pro- 
gresses so  increase  in  dimensions  as  to  eventually  invade  other 
divisions  of  the  vessel.  Thus,  a  sac  at  first  limited  to  the  transverse 
arch  may  in  time  spread  to  the  ascending  portion,  or  one  in  this 
latter  situation  may  at  length  involve  the  entire  arch ;  so  that  both 
subjective  and  objective  symptoms  are  very  liable  to  exhibit 
changes  corresponding  to  the  extension  of  the  aneurysm. 

I  recall  the  case  of  a  locomotive  engineer  w^ho  was  for  many 
months  an  inmate  of  the  Cook  County  Hospital  in  whom  such  a 
change  took  place.  His  aneurysm  at  first  presented  in  such  a  situ- 
ation that  it  was  believed  to  implicate  the  descending  portion  of  the 
arch.  As  months  went  on,  however,  the  tumour  grew  enormously 
towards  the  front,  and  at  the  necropsy  was  found  to  have  involved 
the  entire  arch,  which  had  consequently  lost  all  semblance  to  an 
arch,  being,  in  fact,  but  a  huge  sac  from  heart  to  descending  aorta. 


800  DISEASES  OF  THE   HEART 

Physical  Signs. — Inspection. — In  some  cases  this  is  wholly 
negative,  minute  scrutiny  failing  to  detect  signs  of  pressure,  and 
the  general  appearance  being  that  of  robust  health.  In  other  in- 
stances, on  the  contrary,  patients  look  cachectic,  and  their  chests 
being  uncovered  present  unmistakable  evidence  of  aneurysm.  It 
is  not  to  be  supposed  that  all  the  signs  are  present  in  any  one  case. 
Consequently  the  following  are  the  points  to  be  carefully 
looked  for : 

(1)  Circumscribed  bulging  of  the  chest-wall  in  the  folloAving 
areas:  (A)  At  the  right  of  the  sternum,  especially  in  the  second 
and  third  intercostal  spaces,  but  also  the  first,  and  including  the 
stern o-clavicular  articulation  ;  (B)  at  the  upper  end  of  the  sternum, 
including  the  regions  at  either  side  and  tlio  fossa  jugularis;  (C) 
in  the  intercostal  spaces  at  left  of  the  breastbone,  from  clavicle 
to  fourth  rib ;  (D)  in  the  left  interscapular  region  below  the  level 
of  the  fourth  dorsal  vertebra.  These  are  the  areas  in  which  tho- 
racic aneurysm  most  commonly  makes  its  appearance. 

The  integument  at  these  points  may  appear  smooth  and  shin- 
ing, the  prominence  being  slight,  or  a  tumour  of  such  size  may  pro- 
ject and  have  so  eroded  the  overlying  structures  that  the  skin  is  of 
a  dark  red  or  bluish  hue,  or  may  have  disappeared  in  spots,  leaving 
the  wall  of  the  aneurysm  visible. 

(2)  Signs  of  interference  with  the  circulation:  (A)  visible 
cutaneous  capillaries  on  some  portion  of  the  chest,  as  over  the  area 
of  bulging;  (13)  distended,  tortuous  veins  denoting  the  establish- 
ment of  collateral  circulation  in  consequence  of  pressure  on  some 
of  the  great  internal  veins,  as  superior  vena  cava,  one  of  the  in- 
nominates  or  subclavians;  (C)  localized  (edema,  as  of  one  arm  and 
corresponding  half  of  the  neck,  or  when  bilateral,  of  the  ujipcr 
part  of  the  body,  but  not  of  the  lower  extremities.  Walshe  speaks 
of  the  neck  being  in  some  instances  so  distended  and  spongy  from 
capillary  turgescence  as  to  look  "  like  a  collar  of  flesh." 

(3)  Pulsation  in  some  abnormal  situation — e.  g.,  one  of  the 
areas  in  wliicli  l)nlging  may  appeal-;  or  an  exaggeration  of  a  i)ulsa- 
tion  in  a  normal  situation — e.  g.,  of  the  cervical  arteries,  particu- 
larly on  one  and  not  the  other  side  or  in  the  episternal  notch. 

(4)  Dislocation  of  the  cardiac  impulse,  in  most  instances 
downward  and  to  the  left.  The  organ  may,  however,  be  pushed 
strongly  forward  against  the  anterior  chest-wall. 


ANEURYSM  OF  THE  THORACIC  AORTA  801 

(5)  Diminution  or  absence  of  respiratory  movement  of  one 
half  of  the  thorax,  more  often  the  left,  with,  in  some  cases  of 
marked  bronchial  compression,  also  retraction  of  the  side.  This 
sign  in  conjunction  with  pressare-symptoms  is  highly  suggestive. 

(G)  Immobility  of  one  pupil,  which  may  be  larger  than  its 
fellow,  but  is  more  often  contracted. 

(Y)  Sweating  of  the  head,  sometimes  unilateral,  and  by 
Walshe  said  to  be  very  profuse  in  some  instances.  This  is  another 
sign  of  pressure  on  the  sympathetic,  and  taken  in  conjunction  with 
other  pressure-symptoms  may  be  of  value,  but  found  alone  pos- 
sesses no  significance  as  respects  aortic  aneurysm. 

Palpation  is  of  value  chiefly  as  a  means  of  detecting  abnormal 
pulsation,  its  extent  and  character.  It  is  especially  likely  to  give 
information  when  employed  as  bimanual  palpation,  one  hand 
being  pressed  firmly  against  the  chest  in  front  and  the  other  behind. 
In  this  way,  deeply  situated  pulsation  may  softietimes  be  apj)re- 
ciated  that  otherwise  would  escape  recognition.  If  a  bulging  area 
is  perceived  to  pulsate,  one  should  endeavour  to  feel  the  extent, 
force,  and  direction  of  the  pulsation.  If  the  tumour  is  due  to 
aneurysm,  it  is  likely  that  the  pulsation  includes  the  whole  area. 
If  this  is  forcible,  so  forcible  in  fact  as  to  equal  in  this  regard  the 
beat  of  the  heart,  it  is  highly  suggestive  of  aneurysm  (Balfour). 
Finally,  the  pulsation  of  aneurysm  may  be  slowly  heaving  and  is 
exj)ansile,  and  when  by  palpation  this  character  can  be  determined, 
there  is  no  doubt  of  the  nature  of  the  tumour.  Pulsation  imparted 
to  a  solid  tumour  by  a  vessel  beneath  is  a  simple  forward  thrust 
or  shock. 

In  some  cases  the  hand  laid  iipon  a  tumour  due  to  aneurysm 
perceives  a  distinct  diastolic  shock  which  succeeds  the  systolic  im- 
pulse. This  is  very  characteristic,  being  due  to  elastic  recoil  in  the 
wall  of  the  sac.  In  some  instances  a  thrill  is  detected  in  the  bulg- 
ing area,  but  in  my  experience  is  not  at  all  common,  and  is  of  diag- 
nostic aid  only  in  connection  with  other  signs. 

Palpation  is  of  value  also  in  the  study  of  the  pulse  with  a  view 
to  ascertaining  whether  or  not  it  is  equal  and  synchronous  in  cor- 
responding arteries,  since  when  the  innominate  or  the  left  common 
carotid  and  subclavian  arteries  are  implicated,  smallness  and  per- 
haps retardation  or  obliteration  of  the  pulse  in  the  arteries  of  the 
corresponding  half  of  the  neck  or  arm  are  likely  to  be  occasioned. 


802  DISEASES  OF  THE  HEART 

Palpation  is  of  value  also  in  ascertaining  displacement  of  the  heart, 
as  well  as  hepatic  congestion  due  to  pressure. 

The  finger  pressed  gently  into  the  episternal  notch  may 
sometimes  detect  pulsation  of  the  transverse  arch  of  an  abnor- 
mal character,  or  a  thrill,  as  well  as  the  jogging  impulse  of 
aneurysm. 

The  tracheal  tug  is  another  iihenomenon  sometimes  elicited  by 
palpation.  It  is  a  distinct  downward  pull  of  the  trachea  caused  by 
the  impact  of  the  sac  against  the  windpipe  at  its  bifurcation  or 
against  a  main  bronchus,  and  although  feebly  present  in  some  other 
conditions — e.  g.,  free  aortic  regurgitation — is  never  so  marked  as 
in  aneurysm  of  the  transverse  arch.  To  elicit  tracheal  tugging  the 
examiner  instructs  the  patient  to  raise  his  chin  so  as  to  strongly 
extend  the  neck,  whereupon  he  inserts  the  tips  of  his  forefingers 
into  the  notch  between  the  thyroid  and  cricoid  cartilages  and  pulls 
gently  upward.  If  the  sign  sought  for  is  present,  the  trachea  is 
felt  to  be  jerked  distinctly  downward  with  each  cardiac  systole. 
When  well  marked,  this  tug  cannot  be  mistaken,  but  when  not  pro- 
nounced considerable  care  is  required  for  its  detection. 

Percussion  is  a  valuable  means  of  diagnosis  in  cases  of  aneu- 
rysm, especially  when  there  is  no  visible  tumour.  Before  the  sac 
leads  to  protrusion  of  the  chest-wall  it  may  occasion  retraction  of 
a  lung-border  or  more  or  less  collapse  of  a  lobe,  so  that  dulness  in 
one  of  the  areas  in  which  aneurysm  is  usually  situated  may  be  de- 
tected by  firm  percussion  and  form  an  early  sign  of  such  tumour. 
It  is  especially  important  to  percuss  carefully  in  the  right  infracla- 
vicular region  close  to  the  sternum,  since  loss  of  resonance  in  this 
location  is,  together  with  symptoms  and  signs  of  pressure,  strongly 
suggestive  of  aneurysm.  Dulness  over  the  manubrium  is  not  so 
suggestive  as  at  either  side.  Percussion  is  necessary  also  for  the 
recognition  of  pressure  eifects  on  the  lungs  and  of  displacement  of 
the  heart. 

Auscultation. — Aneurysms  do  not  always  produce  acoustic  phe- 
nomena, a  statement  which  applies  to  some  large  as  well  as  small 
ones  that  are  deeply  situated.  A  sac  may  be  filled  with  coagula, 
and  be  thus  to  all  intents  and  purposes  the  same  as  a  solid  growth, 
in  wbic'li  event  no  adventitious  sounds  are  generated  and  the  aneu- 
rysm remains  silent. 

In    most    instances,    however,    aneurysms    occasion    abnormal 


ANEURYSM   OF   THE   THORACIC   AORTA  803 

sounds  or  bruits  which  ar(;  UTuIible  over  the  sac  or  in  some  neigh- 
bouring vessel  or  part  to  whicli  they  are  propagated. 

There  is  no  auscultatory  phenomenon  pathognomonic  of  aneu- 
rysm, but  certain  sounds  are  more  suggestive  than  are  others.  The 
two  tones  normally  heard  over  one  of  the  great  vessels  at  the  base 
of  the  neck  and  in  the  aortic  area  are  usually  altered  by  the  devel- 
opment of  aneurysm.  Either  the  systolic  or  the  diastolic  may  be 
modified — i.  e.,  intensified,  diminished,  or  impure. 

Perhaps  the  most  frequent  and  striking  change  is  a  loud  pecul- 
iarly ringing  quality  of  the  second  tone  heard  over  the  growth  or  in 
one  of  the  cervical  arteries  but  not  the  others.  In  some  instances 
such  a  sound  is  impure  or  split,  in  others  it  is  clear  and  clanging, 
while  the  first  is  not  pure  or  has  been  replaced  by  a  murmur  of 
harsh  quality.  In  other  cases  again  the  systolic  tone  is  pure  and 
accentuated  and  the  diastolic  is  accompanied  or  obscured  by  a  dis- 
tinct bruit,  while  in  still  others  there  is  a  double  to-and-fro  murmur 
of  wide  propagation. 

Intensification  or  modification  of  the  normal  vascular  sounds 
occurring  in  immediate  proximity  to  the  heart — e.  g.,  in  the  aortic 
area,  are  not  so  suggestive  as  are  such  changes  in  regions  in  which 
they  do  not  normally  exist — e.  g.,  the  left  interscapular  region  or 
one  side  of  the  neck.  Another  very  valuable  auscultatory  sign  is 
the  propagation  of  the  heart-tones  to  a  much  greater  distance  than 
normal — e.  g.,  to  the  outer  limit  of  an  infraclavicular  region  or 
into  an  axilla,  the  lung  tissue  not  being  indurated.  This  condition 
is  essential,  for  solidification  of  lung  from  tuberculosis  may  lead  to 
wide  transmission  of  the  cardiac  sounds  without  aneurysm. 

We  do  not  yet  understand  the  conditions  wdiich  determine 
changes  of  one  kind  and  another  in  the  tones  heard  over  an  aneu- 
rysm. These  sounds  are  probably  not  generated  de  novo  in  the  wall 
of  the  sac,  but  are  merely  conducted  thither  from  the  heart  and 
are  there  intensified,  reduplicated,  or  otherwise  modified  by  vibra- 
tions set  up  in  the  sac-wall  or  by  some  other  condition  that  escapes 
our  ken.  It  may  well  be  that  bruits  are  generated  in  some  cases  in 
the  sac  itself  in  consequence  of  the  blood-stream  swirling  into  or 
out  of  the  sac,  but  probably  the  murmur  is  due  in  other  instances 
to  atheromatous  roughening  of  the  aorta  between  the  heart  and  sac 
or  to  insufficiency  of  the  aortic  leaflets.  This  is  believed  to  be  the 
explanation  of  the  double  aortic  bruit  not  infrequently  heard  in 


804  DISEASES  OP   THE   HEART 

aneurysm  of  the  ascending  portion  of  the  arch.  Indeed,  Gibson 
states  that  lie  can  recall  only  three  cases  in  the  literature  in  which 
such  a  double  bruit  was  found  without  associated  incompetence  of 
the  semilunar  valves.  It  is  not  strange,  therefore,  that  all  possible 
combinations  of  tones  and  murmurs  may  be  heard  in  cases  of  intra- 
thoracic aortic  aneurysm. 

Drummond  has  called  attention  to  the  fact  that  the  pulsation  of 
an  aneurysm  may  be  communicated  to  the  trachea  and  manifested 
by  rhythmical  interruption  of  the  expiratory  murmur.  This  is 
perceived  by  placing  the  stethoscope  upon  the  manubrium  and  aus- 
cultating while  the  patient  exi)ires  slowly  through  only  one  nos- 
tril, the  other  being  closed  by  his  finger.  This  phenomenon  is  not 
peculiar  to  aneurysm,  being  perceived  in  health,  but  is  more  pro- 
nounced. 

In  some  cases  an  aneurysmal  bruit  may  be  ])laiuly  heard  when 
the  bell  of  the  stethoscope  is  placed  between  the  patient's  teeth,  his 
lips  being  closed  about  the  instrument,  Sansom  speaks  of  having 
thus  been  able  to  detect  a  systolic  murmur,  and  Dr.  E.  J.  Abbott,  of 
St.  Paul,  has  narrated  to  me  an  instance  in  which  the  detection  of 
such  a  tracheal  bruit  was  the  only  evidence  of  aneurysm  he  could 
discover.  In  Cook  County  Hospital  at  present  writing  is  a  man 
with  aneurysm  in  whom  both  a  systolic  and  diastolic  bruit  can  thus 
be  loudly  heard.  The  phenomenon  is  due  to  the  conduction  of  the 
murmur  to  the  column  of  air  within  the  trachea.  This  sign  may 
be  of  diagnostic  value  in  cases  of  small  sacs  of  the  transverse  arch 
which  are  too  deeply  situated  to  declare  their  presence  by  outward 
pressure-effects. 

Diagnosis. — Under  some  circumstances  the  diagnosis  of  aneu- 
rysm of  the  thoracic  aorta  may  be  made  almost  at  a  glance,  by  the 
discovery  of  an  external  tumour  displaying  the  expansile  pulsa- 
tion and  other  characters  of  an  aneurysm.  There  are  other  cases, 
on  the  contrary,  in  which  the  most  painstaking  examination  fails 
to  positively  establish  the  nature  of  the  malady.  Between  these 
two  extremes  are  to  be  found  cases  which,  although  obscure,  are  yet 
susceptible  of  elucidation  by  minute  investigation  and  by  ex- 
clusion. 

In  a  suspected  case  the  following  points  may  be  considered  of 
diagnostic  importance:  (1)  A  history  of  syphilis  years  before  or 
of  strain,  as  by  occupation,  to  which  some  would  add  chronic  alco- 


ANEURYSM   OF   THE   TIlORArrC   AORTA  805 

holic  excess.  (2)  Age,  the  patient  being  at  or  after  the  middle 
period  of  life.  (3)  The  male  sex,  since  men  are  vastly  more  liable 
to  aneurysm.  (4)  Symptoms  indicative  of  intrathoracic  pressure ; 
as,  (A)  intractable  ])ain  of  the  characters  previously  described; 
(B)  dyspnoea,  especially  if  influenced  by  posture;  (C)  cough  of 
a  brazen  clang,  also  evoked  or  intensified  by  posture;  (D)  dys- 
phagia or  regurgitation  of  food.  These  four  symptoms,  if  all  pres- 
ent, form  a  very  strong  chain  of  evidence  in  favour  of  an  existing 
aneurysm. 

If  to  the  foregoing  history  and  symptoms  the  following  physi- 
cal signs  are  added,  reasonable  doubt  can  scarcely  be  entertained: 
(5)  Bulging,  even  if  slight,  in  some  one  of  the  areas  in  which 
aneurysm  is  likely  to  be  present.  (6)  Dulness  in  one  of  these 
areas  even  without  perceptible  bulging.  (7)  Displacement  of  the 
heart,  most  often  downward  and  to  the  left.  (8)  Some  of  the 
auscultatory  phenomena  already  described,  especially  a  harsh,  aortic 
systolic  bruit  with  a  clanging  second  sound.  If  such  second  tone 
is  split  or  doubled  and  is  heard  most  plainly  or  solely  over  a  dull 
area  or  in  the  cervical  arteries,  especially  if  on  one  side  and  not  on 
the  other,  and  is  accompanied  by  a  diastolic  shock,  the  evidence, 
taken  in  connection  with  pressure-symptoms,  may  be  considered 
almost  conclusive. 

Aside  from  an  external  tumour  having  a  distinctly  expansile 
pulsation  or  a  diastolic  shock,  there  may  be  said  to  be  no  signs  so 
distinctive  as  to  be  pathognomonic.  Diagnosis  is  to  be  found  in 
the  association  of  several  important  signs  rather  than  in  any  one 
alone.  ISTevertheless  attention  may  be  especially  directed  to  what 
Balfour  considers  very  trustworthy  evidence — namely,  a  pulsation 
in  an  aneurysmal  area  equal  in  intensity  to  the  apex-beat,  so  that 
there  may  be  said  to  be  two  areas  of  maximum  impulse.  Even 
this  is  not  absolute,  however ;  for  a  kyphoscoliosis  has  been  known 
to  push  the  convex  portion  of  the  aortic  arch  so  strongly  against 
the  anterior  chest-wall  at  right  of  the  sternum  as  to  simulate,  with 
respect  to  the  force  of  its  pulsation,  a  thoracic  aneurysm. 

Tracheal  tugging  is  a  very  strong  sign  of  aneurysm  of  the  trans- 
verse arch,  especially  in  conjunction  with  other  signs ;  but  as  it  may 
be  produced  by  other  conditions,  it  is  not  infallible. 

Differential  Diagnosis. — This  concerns  especially  the  three  fol- 
lowing diseases,  which  taken  in  order  of  frequency  and  importance 


806  DISEASES  OF  THE  HEART 

are:  (1)  A  solid  intrathoracic  growth — e.g.,  carcinoma  and  the 
varieties  of  sarcoma;  (2)  mediastinal  abscess;  (3)  pulsating  em- 
pyema in  close  contiguity  to  the  base  of  the  heart. 

(1)  Malignant  Tumour. — This  disease  when  situated  wdthin 
the  thorax  occasions  symptoms  of  pressure  so  identical  in  some  re- 
spects with  those  of  aneurysm  that  they  cannot  be  distinguished. 
The  chief  differential  points  are  to  be  found,  therefore,  in  the  his- 
tory and  physical  signs.  As  a  rule,  the  history  is  of  more  rapid 
growth  than  in  aneurysm,  accompanied  by  more  pronounced  ema- 
ciation and  loss  of  strength.  In  the  physical  signs  the  main  dif- 
ferences are  found  in  the  character  of  pulsation,  when  such  exists, 
and  in  the  auscultatory  phenomena. 

A  solid  tumour  occasions  pulsation  which  is  not  expansile,  but 
is  a  forward  impulse,  owing  to  the  circumstance  that  the  growth 
itself  does  not  pulsate,  but  receives  an  impulse  imparted  to  it  by 
the  aorta  or  some  other  artery  or  by  the  heart  against  which  the 
tumour  lies.  More  commonly,  however,  such  a  mass  possesses  no 
impulse.  It  must  not  be  forgotten,  on  the  other  hand,  that  when 
a  sac  is  filled  with  dense  coagula,  it  is  practically  also  a  solid 
tumour,  and  hence  under  such  conditions  may  be  also  incapable  of 
producing  any  perceptible  pulsation.  I  recall  such  an  instance  in 
Cook  County  Hospital.  A  large,  dense,  intensely  resisting,  non- 
pulsating  tumour  protruded  close  to  the  sternum  in  the  right  infra- 
clavicular region.  It  was,  moreover,  perfectly  silent,  and  very 
naturally  was  for  a  long  time  mistaken  for  a  malignant  growth. 
Only  after  the  lapse  of  time  had  somewhat  altered  the  size  of  the 
sac  and  permitted  vascular  sounds  to  be  generated  was  a  correct 
diagnosis  possible. 

As  regards  the  sounds  audible  over  a  solid  tumour,  it  may  be 
stated  that  when  such  are  present  they  are  usually  clear  and  un- 
changed. It  is  possible,  however,  for  the  cardiac  or  vascular  sounds 
to  be  modified  in  consequence  of  pressure  by  the  growth.  Under 
such  circumstances  bruits  may  be  generated  or  the  second  sound 
may  take  on  a  ringing  intensification.  It  is  not  likely  to  be  so 
clanging  as  is  sometimes  the  case  in  aneurysm.  Moreover,  a  tu- 
mour of  the  mediastinum  which,  from  its  situation  and  resulting 
area  of  dulness,  simulates  aneurysm  of  tlie  transverse  arch,  does 
not  occasion  a  tracheal  tug.  Neither  is  such  a  solid  growth  when 
situated  in  the  area  at  right  of  sternum,  and  hence  simulating 


ANEURYSM  OP  THE  THORACIC  AORTA         807 

aneurysm  of  the  ascending  aorta,  likely  to  lead  to  signs  of  insuf- 
ficiency of  the  semilunar  valves.  It  does  not  change  its  direction 
of  growth  and  cause  sudden  modification.^  of  symptoms,  nor  is  it 
apt  to  create  asymmetry  of  the  pulses.  Finally,  in  cases  of  malig- 
nant growths  there  may  be  history  or  symptoms  of  an  ante- 
cedent tumour  elsewhere,  or  there  may  be  induration  of  some  of  the 
lymph-nodes  in  axilla  or  neck  which  may  aid  in  the  correct  inter- 
pretation of  the  case. 

(2)  Mediastinal  Abscess. — In  this  infrequent  affection  there 
is  history  of  more  sudden  invasion,  and  pain  is  an  early  symptom, 
even  before  pressure  has  become  sufficient  to  occasion  dyspnoea. 
Fever  is  likely  to  be  present,  and  is  an  early  symptom,  whereas 
when  it  exists  in  aneurysm  it  is  apt  to  be  late,  after  the  sac  has 
begun  to  exert  pressure  on  the  bronchus  or  lung  with  phthisical 
symptoms.  In  abscess,  moreover,  there  is  not  likely  to  be  the 
change  in  the  vascular  sounds  or  the  production  of  new  ones  as 
occurs  in  aneurysm.  The  disease  may  arise  at  any  age  and  in 
either  sex,  showing  no  predilection  for  the  male  sex. 

(3)  Pulsating  empyema  may  simulate  an  aneurysm  when  an 
empyema  necessitatis  forms  in  close  proximity  to  the  base  of  the 
heart.  It  is,  however,  exceedingly  rare,  and  may  occur  in  children 
as  well  as  in  adults.  The  history  and  examination  of  the  lungs 
ought  to  clear  uj^  the  nature  of  the  case.  Should  a  circumscribed 
empyema  in  immediate  contiguity  to  the  heart  display  bulging 
and  pulsation  as  well  as  dulness,  it  may  occasion  considerable 
difficulty  of  correct  diagnosis,  but  ought  at  length  to  be  diagnosed 
by  exclusion,  if  not  by  history  and  physical  signs  indicative  of  its 
real  nature. 

Other  diseases  producing  signs  in  the  aortic  area — i.  e.,  dila- 
tation of  the  ascending  arch  associated  with  aortic  regurgitation, 
stenosis  of  the  aortic  ostium,  and  sclerosis  of  the  ascending  arch — 
may  and  have  been  mistaken  for  aneurysm.  In  the  case  of  the 
first  mentioned  a  positive  differential  diagnosis  is  sometimes  ex- 
tremely difficult,  when  the  regurgitation  occurs  in  the  male  past 
middle  age,  but  as  a  rule  pressure-effects  are  absent.  Thrill  and 
systolic  murmur  may  in  cases  of  stenosis  give  rise  to  suspicion  of 
aneurysm,  but  error  may  ordinarily  be  avoided  by  study  of  the 
history,  age,  the  second  sound,  the  position  and  size  of  the  heart, 
and  the  characters  of  the  pulse.     Sclerosis  of  the  aorta  may  occa- 


808  DISEASES   OF   THE   HEART 

sion  a  systolic  bruit  and  ringing  second  sound  very  suggestive  of 
aneurysm,  but  does  not  occasion  pressure-effects  noted  in  aneurysm. 
In  all  these  three  affections  the  subsequent  progress  will  probably 
clear  up  the  case. 

Pulmonary  tuberculosis,  fibrosis  and  retraction  of  the  lung  and 
throbbing  of  the  aorta  sometimes  observed  in  neurotic  subjects 
ought  not  to  occasion  material  difficulty  if  due  attention  is  paid 
to  the  history,  symptoms,  and  clinical  findings. 

Formerly  the  sphygmograph  used  to  be  depended  on  to  aid  in 
the  detection  of  thoracic  aneurysm,  and  may  in  favourable  cases 
afford  reliable  information,  by  furnishing  a  tracing  of  one  or  both 
radials  in  which  the  usual  characters  are  wholly  wanting,  but  in 
many  instances  it  fails  to  record  positive  evidence. 

N^owadays  we  are  accustomed  to  resort  to  the  X-ray  in  all 
doubtful  or  suspected  cases.  The  reader  is  referred  for  details  to 
the  appropriate  article  in  the  Appendix. 

Prognosis  may  be  said  to  be  extremely  unfavourable,  for 
although  spontaneous  cure  through  obliteration  of  a  small  sac  or 
one  with  a  narrow  pedicle  sometimes  takes  place,  it  is  unlikely  for 
such  to  happen.  Furthorniore,  the  results  of  medical  or  surgical 
treatment  are  not  encouraging.  The  progress  of  the  disease  is  not 
of  a  necessity  steadily  downward,  although  such  is  apt  to  be  the 
rule.  Remissions  may  occur  both  in  the  gravity  of  subjective 
symptoms  and  growth  of  the  sac. 

Thoracic  aneurysm  may  run  a  comparatively  rapid  course,  par- 
ticularly if  the  sac  develops  externally  and  ruptures,  but  the  dis- 
ease may  persist  for  years,  depending  of  course  upon  the  size,  direc- 
tion of  growth,  and  physical  conditions  of  the  sac.  Ten  years  may 
be  said  to  be  a  long  period  of  time  for  the  continuance  of  thoracic 
aneurysm,  and  yet  this  limit  has  been  reached  and  even  surpassed. 
Finally,  the  outlook  is  influenced  largely  by  the  habits,  general 
status,  and  environment  of  the  individual,  the  same  as  in  any  other 
form  of  cardiac  or  vascular  disease. 

Modes  and  Causes  of  Death. — The  fatal  termination  may 
be  said  to  occur  either  from  rupture  or  tlio  dirc'ct  or  indirect  effects 
of  pressure.  Death  from  rupture  is  not  the  most  frequent  mode  of 
termination,  as  shown  by  Hare's  and  Holder's  figures,  previously 
quoted,  according  to  which  it  was  the  cause  of  death  in  289  out  of 
953  cases.    Rupture  may  take  place  externally  or  into  any  one  of 


ANEURYSM   OP   THE   THORACIC   AORTA  809 

the  contiguous  structures,  pericardium,  heart,  pleural  cavity, 
bronchus,  trachea,  a'soplmgus,  'vena  cava,  pulmonary  artery.  In 
such  an  event  death  nuiy  be  immediate  or  protracted  over  a  period 
of  hours. 

More  commonly,  life  is  terminated  in  consequence  of  mechani- 
cal interference  with  respiration  or  circulation  and  cardiac  inade- 
quacy, or  the  patient  succumbs  to  "  aneurysmal  phthisis  "  or  gen- 
eral exhaustion  and  cachexia.  Under  such  circumstances  the  end 
may  come  slowly  or  suddenly  after  weeks  of  slowly  progressing  loss 
of  strength.  The  last  hours  are  in  many  cases  fraught  with  ex- 
treme suffering  and  death  is  hailed  as  a  blessed  deliverer. 

Treatment. — The  not  infrequent  post-mortem  discovery  of 
the  spontaneous  cure  of  thoracic  aneurysm  by  coagulation  of  the 
blood  within  the  sac  has  furnished  the  hint  upon  which  all  thera- 
peutic measures  are  based  that  aim  at  anything  more  than  pallia- 
tion of  symptoms.  The  accomplishment  of  this  object  presupposes 
certain  favouring  conditions  in  the  sac  itself.  In  the  first  place 
the  aneurysm  must  be  of  the  saccular  variety,  and  in  the  second  it 
must  communicate  with  the  aorta  by  a  narrow  opening.  Given 
these  essentials,  it  is  possible  for  clotting  within  the  sac  to  take 
place. 

If  these  conditions  are  not  present,  there  is  little  or  no  prospect 
of  cure,  and  medical  skill  is  powerless  to  do  more  than  mitigate 
suffering  or  furnish  advice,  which  if  carried  out  may  retard  prog- 
ress. In  the  majority  of  cases,  unfortunately,  we  are  compelled  to 
content  ourselves  with  palliative  measures  and  watching  the  course 
of  the  disease. 

Our  aim  should  be,  however,  to  effect  a  cure  in  every  case  in 
which  there  seems  to  be  such  a  possibility.  Consequently,  the  first 
measure  to  be  advised  is  rest  in  the  recumbent  'position.  The  object 
of  this  plan  of  management  is  the  reduction  in  the  number  and  force 
of  cardiac  contractions  that  thereby  the  flow  of  blood  within  the 
aneurysm  may  be  less  swift.  Ever  since  its  introduction  by  Val- 
salva the  value  and  importance  of  this  measure  has  been  recognised. 
To  be  effective  the  rest  must  be  absolute  and  must  include  rest  of 
mind  as  well  as  of  body.  Whatever  excites  the  heart  to  more  rapid 
and  powerful  systoles  must  be  avoided,  and  to  attain  as  complete 
rest  as  is  necessary,  the  patient  should  be  clearly  instructed  con- 
cerning its  advantages  and  necessity. 


810  DISEASES   OF   THE   HEART 

It  is  also  advisable  that  arterial  tension  be  reduced  and  the  vol- 
ume of  the  blood  diminished.  To  this  end  the  diet  must  be  re- 
stricted, as  was  recommended  by  Tufnell,  of  Dublin.  His  dietary 
was  extremely  rigid,  consisting  as  it  did  of  2  ounces  of  bread  and 
butter  with  2  ounces  of  milk  for  breakfast  and  supper  alike,  while 
for  the  midday  meal  2  to  3  ounces  of  meat  and  3  to  4  ounces  of 
milk  were  allowed. 

Such  a  rigid  restriction  in  the  amount  of  food  requires  for  its 
successful  carrying  out  courage  and  determination  on  the  part  of 
the  patient,  and  few  persons  will  submit  to  such  an  almost  starva- 
tion diet.  It  is  probable  that  the  daily  allowance  may  be  somewhat 
greater  than  Tufnell's  dietary  permitted  without  destroying  the 
aim  of  treatment,  provided  one  remembers  that  if  blood-pressure 
is  to  be  lowered  the  quantit}^  of  fluid  allowed  must  be  small.  Fur- 
thermore, if  such  management  is  to  accomplish  results  it  must 
be  persevered  in  for  several  months  or  until  the  aneurysm  gives 
evidence  of  having  diminished  in  size.  While  carrying  out  this  or 
any  other  mode  of  treatment  the  bowels  are  to  be  kept  freely  open 
that  there  may  be  no  straining  at  stool  or  increase  of  blood-pressure 
incident  to  constipation. 

The  next  plan  of  management  that  promises  beneficial  results  is 
the  administration  of  iodide  of  potassium.  This  mode  of  treatment 
was  at  very  nearly  the  same  time  recommended  by  Bouillaud  and 
Chuckerbutty,  but  has  been  especially  advocated  by  Balfour.  It 
is  not  advised  because  of  the  syphilitic  history  obtained  in  most 
cases  of  thoracic  aneurysm,  but  for  the  purpose  of  influencing  the 
sac  in  some  as  yet  unknown  manner.  Balfour  is  of  the  opinion 
that  this  salt  leads  to  thickening  and  contraction  of  the  aneurysmal 
wall,  while  others  believe  its  beneficial  action  lies  in  decrease  of 
blood-pressure  and  slowing  of  the  heart's  action.  \. 

Whatever  be  its  modus  operandi,  it  is  not  necessary  and  it  is 
not  advised  to  prescribe  enormous  doses,  as  used  to  be  done,  but  to 
administer  it  in  doses  of  5,  10,  or  15  grains  thrice  daily,  since  these 
moderate  doses  accomjolish  exactly  as  much  as  do  larger  ones.  The 
dose  of  the  salt  must  not  be  large  enough  to  produce  acceleration 
of  the  pulse,  the  rate  of  which  during  repose  should  have  been  pre- 
viously determined.  The  remedy  should  be  continued  for  many 
months,  and  is  advantageously  combined  with  rest  and  a  restricted 
diet. 


ANEURYSM  OF  THE  THORACIC  AORTA         811 

Testimony  is  universal  tha,t  the  first  and  ^jronounced  effect  is 
relief  or  very  considerable  amelioration  of  pain  due  to  the  aneu- 
rysm. Why  this  is  cannot  be  said,  but  there  can  be  no  doubt  of 
the  empirical  fact.  This  plan  of  management  should  be  instituted 
in  all  cases,  yet  to  promote  a  cure  of  the  disease  favourable  condi- 
tions of  the  sort  explained  above  must  be  present  in  the  tumour. 

The  foregoing  are  the  simplest  measures,  and  in  most  instances 
are  likely  to  accomplish  as  much  as  any  other  of  the  various  plans 
of  management  that  have  been  recommended  and  will  now  be 
mentioned. 

The  surgical  procedures  sometimes  employed  in  the  treatment 
of  this  formidable  complaint  are  five  in  number,  as  follows: 

(1)  The  introduction  into  the  interior  of  the  sac  of  many 
feet  of  fine  iron  or  steel  wire,  horsehair,  catgut,  or  silk  thread. 
The  object  of  such  treatment  is  the  coagulation  of  the  blood  in  the 
meshes  of  this  foreign  material,  wire  being  preferable  to  the  others. 
This  operation,  known  as  the  Moore  or  Loreta  method,  has  been 
done  a  number  of  times,  but  not  with  sufficiently  brilliant  results 
to  make  it  a  popular  mode  of  treatment.  Of  the  16  cases  collected 
by  White  and  Gould  (Gibson),  only  2  were  successful,  while  of  the 
8  cases  of  thoracic  aneurysm  so  treated  and  collected  by  Hunner 
prior  to  1900  (Osier),  all  died.  The  great  objection  to  this  method 
of  management  is  the  resulting  inflammation  and  aggravation  of 
the  condition. 

(2)  Electrolysis,  which  consists  in  passing  a  galvanic  current 
through  the  contents  of  the  aneurysm  by  means  of  two  insulated 
needles  introduced  through  the  wall  of  the  sac.  The  points  of  the 
needles  are  to  be  left  uncovered  by  the  insulating  material.  They 
must  not  be  in  contact  when  inside  the  tumour.  The  electrical 
current  thus  applied  causes  coagulation  of  the  sac  contents,  and  in 
Gibson's  opinion  promises  well,  although  the  results  as  yet  have  not 
been  very  satisfactory.     It  is  worthy  of  trial  in  suitable  instances. 

(3)  The  Moore-Corradi  method,  which  consists  in  the  combi- 
nation of  the  two  procedures  just  mentioned.  A  fine  gold,  silver, 
or  steel  wire  is  passed  into  the  sac,  and  then  a  galvanic  current  is 
sent  through  the  wire.  This  method  is  said  to  have  yielded  sat- 
isfactory results  in  a  few  instances.  It  has  been  performed  by 
Burresi  and  Hershey.  Of  17  cases  of  thoracic  aneurysm  thus 
treated  prior  to  1900  only  3  were  successful.     According  to  Hun- 


812  DISEASES  OF  THE  HEART 

ner,  this  method  is  not  devoid  of  the  following  dangers:  (1) 
embolism;  (2)  the  formation  of  a  secondary  bulging  of  the  wall 
of  the  sac;  and  (3)  obliteration  of  an  artery  springing  from  the 
wall  of  the  aneurysm. 

(4)  The  scratching  of  the  inner  surface  of  the  sac-wall  with 
the  point  of  a  thoroughly  sterilized  needle,  a  method  said  to  have 
been  introduced  by  Macewen  (Gibson).  After  the  integument 
has  been  carefully  sterilized  an  aseptic  needle  is  passed  through 
into  the  aneurysm  until  its  point  comes  in  contact  with  the  internal 
surface  at  the  opposite  side.  The  needle  may  then  be  left  m  situ 
to  be  moved  about  and  made  to  scratch  the  lining  of  the  sac  by  the 
pijlsations  of  the  aneurysm,  or  the  surgeon  may  irritate  the  wall 
by  moving  the  point  of  the  needle  about  first  in  one  place  and 
then  in  another,  but  without  removing  the  instrument.  If  the 
needle  is  left  in  situ,  it  should  not  be  allowed  to  remain  for  longer 
than  twenty-four  to  thirty-six  hours.  This  method  is  simple,  said 
to  be  safe,  and  to  promise  well. 

(5)  The  subcutaneous  injection  of  a  1-per-cent  solution  of  pure 
white  gelatin  in  normal  salt  solution.  This  method  was  introduced 
by  Lancereaux  in  1896,  and  by  him  was  highly  praised.  At  first 
a  2-per-cent  solution  Avas  employed,  but  at  ^lio  suggestion  of  Hu- 
chard  was  reduced  to  half  this  strength  as  being  safer. 

The  gelatin  solution  should  be  carefully  filtered  and  sterilized 
under  pressure  at  the  temperature  of  120°  C.  Two  hundred  or 
250  cubic  centimetres  of  this  1-per-cent  solution  at  a  temperature 
of  about  100°  F.  are  to  be  very  slowly  injected  into  the  loose 
subcutaneous  tissue  of  the  thigh  or  abdomen,  after  which  the 
patient  is  to  be  kept  perfectly  quiet. 

Injections  should  be  repeated  every  six  to  eight  days  until  20 
in  all  have  been  given.  The  objections  to  this  plan  of  treatment 
are  the  intense  pain  and  sometimes  local  and  general  reaction  that 
follow.  In  the  case  of  the  patient  treated  in  this  manner  by  Dr. 
Carl  Beck,  and  previously  mentioned  in  these  pages,  the  tempera- 
ture rose  to  101°  F.  or  thereabouts  after  the  injections. 

Cures  have  been  reported  in  France,  but  in  this  country,  so  far 
as  I  know,  the  results  have  been  unsatisfactory.  It  may  be  tried 
in  desperate  cases;  but  so  many  difiiculties  and  dangers  attend  its 
use,  that  it  is  not  likely  to  become  widely  employed.  Among  the 
dangers  is  the  risk  of  sepsis  or  tetanus,   since   10   per  cent  of 


ANEURYSM  OF  THE  THORACIC  AORTA         813 

comiTiercial  gelatin  is  .said  to  contain  germs,  especially  the  tetanus 
bacillus.  Moreover,  not  many  patients  will  be  found  willing  to 
bear  the  pain  from  the  injections  and  the  subsequent  febrile  re- 
action. Finally,  of  the  cases  in  which  this  treatment  has  been 
tried,  but  a  small  percentage  has  shown  really  encouraging  results. 
The  use  of  gelatin  in  this  manner  does  not  ap})ear  to  increase  the 
coagulability  of  the  blood,  and  since  the  action  is  as  yet  not  under- 
stood, it  has  been  suggested  that  the  remedy  be  given  by  the  mouth 
as  food,  15  grammes  being  consumed  daily. 

When  one  considers  the  pathology  of  thoracic  aneurysm,  the 
great  internal  pressure  to  which  the  wall  of  the  sac  may  be  sub- 
jected in  cases  in  which  the  mouth  of  the  aneurysm  is  a  wide  one, 
and  usually  the  advanced  stage  of  the  process  when  the  individual 
applies  to  the  surgeon  for  relief,  it  is  not  strange  that  failure,  or 
at  best  only  amelioration,  of  symptoms  follows  any  attempt  at 
a  cure. 

The  most  that  can  be  done  in  the  great  majority  of  cases  is  to 
mitigate  the  patient's  distress.  If  the  iodide  of  potash  does  not 
relieve  the  pain,  recourse  must  be  had  to  opium  in  some  form. 
Subcutaneous  injections  of  morphine  are  the  best^  since  they,  not 
only  rid  the  sufferer  of  his  pain  for  a  time,  but  they  also  lessen 
his  sense  of  dyspnoea  and  promote  sleep.  I  have  not  yet  prescribed 
heroin  in  a  case  of  aneurysm,  but  think  it  ought  in  the  dose  of 
one-twelfth  grain  not  only  to  prove  efficient  against  the  cough,  but 
should  diminish  the  sense  of  dyspna3a. 

Venesection  is  highly  recommended  for  relief  of  venous  con- 
gestion and  to  decrease  blood-pressure  for  a  time,  and  thereby  the 
dull  pain  arising  from  pressure  within  the  sac.  Only  a  few  ounces, 
3  to  5,  should  be  taken  at  a  time,  since  it  may  have  to  be  frequently 
repeated,  and  the  abstraction  of  too  much  would  only  serve  to 
w^eaken  the  patient  without  doing  more'  good  than  do  the  few 
recommended. 

When  the  sac  is  external  and  large,  it  is  said  to  minister  to  the 
patient's  comfort  to  have  him  wear  an  elastic  bandage  over  the 
tumour  (Osier).  It  certainly' ought  to  lessen  the  tension  to  which 
the  integument  and  thoracic  parietes  may  be  subjected,  and  thereby 
mitigate  pain.  In  some  cases  it  may  be  necessary  to  protect  the 
tumour  against  violence  from  external  blows  by  having  the  patient 
wear  a  shield  of  thin  metal  or  woven  wire  strapped  to  his  chest. 


814  DISEASES  OF   THE   HEART 

The  diet  of  these  sufferers  should  be  light,  eveu  though  they  are 
not  placed  at  complete  rest,  and  they  should  never  be  allowed  to 
become  constipated,  since  straining  at  stool  is  sure  to  prove  harm- 
ful. They  should  take  a  daily  laxative,  and  now  and  then,  when 
blood-pressure  becomes  too  high,  they  should  receive  a  sharp  purge 
from  calomel. 

They  should  be  informed  of  the  dangerous  nature  of  their 
malady  and  be  warned  of  the  risk  attending  severe  physical  efforts, 
excitement,  excesses,  etc. 

There  are  times  when  from  cardiac  inadequacy  digitalis  or 
one  of  its  congeners  may  appear  indicated,  but  one  should  remem- 
ber that  such  agents  are  likely  to  injure  rather  than  benefit  the 
aneurysm.  Consequently  if  such  a  remedy  is  called  for,  it  should 
be  administered  with  caution  and  its  effects  should  be  carefully 
watched. 

When  at  length  it  is  plain  that  the  end  is  near,  and,  as  it 
approaches,  suffering  is  intense,  I  am  of  the  opinion  that  the  phy- 
sician is  warranted  in  the  free  administration  of  morphine  injec- 
tions to  promote  euthanasia.  I  certainly  should  not  hesitate  under 
such  circumstances  to  inject  a  dose  that  would  hasten  the  patient's 
death.  I  know  of  an  instance  in  which  this  was  done  to  prevent 
the  terrible  shock  to  the  friends  that  was  sure  to  follow  the  impend- 
ing rupture  of  a  large  external  sac. 


APPENDIX 


MECHANICAL    DEVICES    AS    AIDS    TO    DETERMINING 
CARDIAC    DISEASE 

THE   X-RAY 

Peecussiotst  and  auscultation  are  not  entirely  satisfactory 
methods  of  examining  the  heart,  for  the  reason  that  thick,  rigid 
parietes,  pulmonary  emphysema,  or  other  conditions  may  prove 
sources  of  error.  Much  depends  also  on  the  skill  of  the  examiner 
or  on  his  delicacy  of  hearing,  so  that  it  is  quite  common  for  two  or 
more  examiners  to  obtain  results  that  do  not  wholly  agree.  When, 
therefore,  the  Roentgen-ray  came  into  use  it  was  quite  naturally 
hoped  it  would  furnish  a  reliable  means  of  detecting  diseased  con- 
ditions in  the  heart. 

Accordingly,  considerable  work  along  this  line  has  been  done 
both  in  Europe  and  this  country.  As  a  result  of  such  investiga- 
tions we  now  know  that  the  X-ray  is  in  many  cases  a  valuable  aid 
to  the  diagnosis  of  internal  diseases,  but  cannot  altogether  replace 
other  and  older  means  of  investigation.  This  is  pre-eminently  true 
of  cardiac  disease. 

Francis  P.  Williams,  of  Boston,  is  a  particularly  diligent  in- 
vestigator with  the  X-ray,  and  it  is  to  his  elaborate  paper  in  the 
Philadelphia  Medical  Journal  of  January  6,  1900,  that  I  am  in- 
debted for  much  of  what  is  here  stated.  Percussion  of  the  cardiac 
area  was  made  by  Williams  and  his  friends  in  a  large  series  of  cases 
both  healthy  and  diseased,  and  after  the  limits  of  deep-seated  dul- 
ness  had  been  carefully  marked  out  on  the  bare  skin  the  results 
thus  obtained  were  compared  with  those  of  the  X-ray  by  means  of 
the  fluorescent  screen.  The  conclusion  Williams  arrived  at  was 
that  the  fluoroscope  is  a  much  more  trustworthy  means  of  judging 
of  the  size  of  the  heart.    He  found  that  in  normal  hearts  the  dis- 

815 


816  DISEASES  OF  THE  HEART 

crepancies  between  percussion  and  the  fliioroscope  were  not  so 
marked  as  when  the  heart  was  either  undersized  or  oversized,  and 
that  the  greater  the  enlargement  of  the  organ  over  the  normal,  the 
less  frequent  is  the  error  by  percussion,  although  the  more  pro- 
nounced is  such  error  when  made. 

He  furthermore  discovered  the  X-ray  to  be  a  more  precise 
method  of  determining  the  shape  and  position  of  the  heart. 
Thus  Williams  found  that  in  one  case,  in  which  the  situation 
of  the  apex-beat  and  the  results  of  percussion  led  him  to  conclude 
that  the  heart  was  hypertrophied,  the  X-ray  showed  the  organ  to 
be  merely  displaced  downward  so  as  to  lie  transversely.  Trans- 
positions are  also  discovered  by  means  of  the  fluorescent  screen 
more  certainly  than  by  percussion.  This  was  brought  out  very 
clearly  in  cases  of  left-side  pleuritic  effusions. 

Congenital  malformations  are  stated  to  be  capable  of  diagnosis 
by  the  X-ray,  and  by  this  means  patency  of  the  ductus  arteriosus 
has  been  determined.  It  also  enables  one  to  diagnosticate  a  peri- 
cardial effusion,  as  is  well  illustrated  by  the  figure  opposite  kindly 
furnished  me  by  W.  C.  Fuchs,  who  took  the  skiagraph  from  which 
the  cut  has  been  made  (Fig.  118).  Cardiac  contractions  can  be 
observed  and  differences  in  size  between  systole  and  diastole  noted, 
particularly  in  cases  of  valvular  incompetence. 

The  value  of  the  X-ray  in  the  diagnosis  of  aortic  aneurysms  has 
been  repeatedly  proved.  Williams  finds  that  certain  aneurysms 
can  be  more  surely  detected  by  this  means  than  by  any  other  mode 
of  examination.  It  enables  one  to  determine  their  location  and 
extent  and  whether  or  not  the  tumour  is  increasing  in  size.  Final- 
ly, if  the  aneurysm  is  situated  at  the  left,  it  is  best  seen  from 
behind,  while  those  at  the  right  of  the  heart  show  best  from  the 
front.  Although  it  is  possible  for  even  skilled  observers  to  commit 
error  by  incorrectly  interpreting  normal  pulsations  seen  by  aid  of 
the  fluoroscope,  still  there  can  be  no  doubt  of  the.  positive  value 
of  the  X-ray  in  this  class  of  cases. 

To  sum  up,  it  may  be  stated  that  aside  from  the  detection  and 
study  of  aneurysms  the  real  practical  value  of  the  X-ray  in  cardiac 
disease  lies  in  its  greater  accuracy  in  determining  the  size  of  the 
heart  in  general,  enlargement  of  any  of  the  chambers,  displace- 
ments and  transpositions  and  certain  obscure  congenital  malforma- 
tions.   Even  if  it  could  replace  percussion  and  auscultation,  which 


818  DISEASES   OF   THE   HEART 

it  cannot,  its  lack  of  portability  would  preclude  the  possibility  of 
its  supplanting  older  methods. 

THE  SPHYGMOGRAPH 

The  sphygmograph  is  at  tlie  same  time  one  of  the  most  useful 
and  most  useless  of  the  instruments  used  in  clinical  medicine.  If 
used  as  a  routine  in  his  practice  by  the  observing  physician  it  will 
exceed  in  value  the  feeling  of  the  pulse  by  the  fingers,  which  it 
should  supplement  and  not  supplant.  The  educated  tactile  sense, 
which  is  always  quickly  and  easily  available,  can  appreciate  nearly 
everything  which  the  sphygmograph  can  show,  and  some  features 
which  this  instrument  is  unable  to  delineate,  but  the  impressions 
cannot  be  intelligently  described  and  are  evanescent.  On  the  con- 
trary, the  sphygmograph,  which  is  not  always  at  hand  nor  readily 
applicable,  can  graphically  show  nearly  everything  that  the  finger 
can  detect  and  some  characteristics  which  this  member  cannot 
appreciate,  and  the  results  may  be  preserved  for  deliberate  study, 
comparison,  future  reference,  and  exhibition  to  others. 

The  clinician  will  be  able  to  do  good  work  with  any  one  of  the 
standard  sphygmographs,  but  he  can  use  with  the  greatest  facility, 
and  can  interpret  most  readily  and  accurately  the  tracings  made 
by  the  instrument  with  which  he  is  most  familiar.  My  own  pref- 
erence is  for  Dudgeon's  sphygmograph,  which,  because  of  its  por- 
tability and  adaptability,  readily  lends  itself  to  the  exigencies  of 
all  kinds  of  practice. 

In  the  practical  application  of  the  sphygmograph  certain  ele- 
mentary rules  must  be  followed,  but  the  whole  secret  of  success  in 
manipulating  the  instrument  lies  in  placing  and  maintaining  the 
metal  pad  upon  the  artery  in  such  manner  as  to  give  the  greatest 
possible  amplitude  to  the  excursions  of  the  lever.  The  wrist  band 
should  be  elastic ;  the  pad  properly  placed ;  the  tension  correctly 
adjusted  ;  the  pressure  gauged  to  give  the  greatest  amplitude  to 
the  writing  lever.  In  adjusting  and  maintaining  the  instrument 
in  proper  position  it  is  essential  that  the  operator  should  rely, 
mainly,  upon  his  fingers  and  not  upon  mechanical  appliances. 
Facility  in  the  use  of  the  sphygmograph  can  only  be  attained  by 
practice. 

It  may  be  noted  that  the  most  convenient  strips  of  paper  which  can  be 
used  are  made  from  ordinary  heavy  writing  paper,  cut  thirty-one  thirty-seconds 


THE  SPHYGMOGRAPH 


819 


of  an  inch  wide,  and  blackened  with  smoke  from  burning  camphor.  The  best 
varnish  for  preserving  the  tracirfgs  is  the  ordinary  sandarac  varnish  used  by 
dentists,  suitably  thinned  by  the  addition  of  absolute  alcohol. 


Fig.  119. — From  a  IIealtiiy  Man,  Forty-five  Years  of  Age. 

Tracings  of  the  normal  pnlse  in  health  vary  infinitely  in 
their  characteristics,  and  no  two  are  ever  exactly  alike.  The  above 
sphygmogram  (Fig.  119)  may  be  considerecl  fairly  typical  of  the 
pulse  in  the  healthy  middle-aged  adult. 


Fig.    120. — -From   a   Womaw,  Aged   Forty-four,  During   an   Attack    of    Paroxysmal 
Tachycardia.    Pulse,  196  per  Minute. 

Between  the  extreme  frequency  of  the  pulse  in  paroxysmal 
tachycardia  and  the  remarkable  slowness  of  bradycardia  lies  a 
wide  gap  which  is  filled  by  the  rapid  pulses  of  infectious  fevers, 
the  varying  pulses  of  health  and  the  slow  pulses  of  age,  some  of 
the  intoxications,  etc.  (Figs.  120  and  121). 


Fig.  121. — From  a  Man,  Aged  Twenty-eight,  -with  Eecuerent  Bradycardia.    Pulse, 

25  per  Minute. 

The  sustained  arterial  tension  as  shown  in  the  pulse  varies 
within  wide  limits.  The  lowest  tension  is  found  in  some  of  the 
acute  infections — e.  g.,  general  gonorrhoeal  or  pneumococcal,  in 
which  there  occurs,  very  early,  profound  capillary  paresis.  In 
many  of  these  cases  the  powerful  left  ventricle  throws  the  blood 


820  DISEASES  OP   THE   HEART 

forcibly  into  the  arteries  and  tlirouiili  the  capillaries  with  prac- 
tically no  resistance,  as  shown  in  the  following  tracing  (Fig.  122). 


Fig.  12i!. — Fkum  a  Man,  AbEu  Tweniy-five,  with  Acute  Genekal  Gonouuhceal 

Infection. 

In  some  of  these  cases  the  capillary  and  arteriole  vaso-motor 
reflexes  respond  energetically  to  an  nnnatnral  stinmlns,  and  the 
dicrotic  pnlse  of  every  grade  is  the  result,  an  example  of  which  is 


Fig.  l2o. — FuoM  a  Man,  Aukd  Foinv,  with  Declining  Tvimiuid  Fever. 

given  in  Fig.  123.  The  hyperdicrotic  pnlse,  as  shown  in  Fig.  124, 
is  so  often  seen  in  ha?morrhages  accompanied  by  nervous  excite- 
ment— e.  g.,  in  ha?moptysis — that  it  may  be  considered  somewhat 
distinctive. 

In  aortic  regurgitation  the  po^verful  left  ventricle  vigorously 
propels  a  large  volume  of  blood  into  nearly  collapsed  arteries, 


Fig.  124. — liyrEKDiuKoxic   Fllue   fkom   a   Woman,  Aoeu    Tiiiuty-kive,  aktek   Twelve 
Hours  Kecurkino  ILemoptvsis.    Pulse,  135. 

quickly  and  Avidely  distending  tlieni,  but  the  flow  of  blood  through 
the  capillaries,  during  and  immediately  following  the  systole,  and 
the  reflux  of  blood  through  the  open  valve,  the  instant  ventricu- 


THE  SPHYGMOGRAPH 


821 


lar  action  ceases,  as  quicklj-  reduce  the  arterial  tension,  and  the 
typical  pulse  of  this  condition  is  the  result,  as  shown  in  Fig.  125. 


Fig.  125. — Fkom  a  Woman,  Aged  Twenty-five,  with  Mouekate  Aoktic   Insufficiency, 

Well  Compensated. 

In  this  connection  it  should  be  remembered  that,  other  conditions  being 
equal,  the  pulse  will  be  less  frequent  and  approximate  the  normal  in  character, 
or  more  frequent  and  with  exaggeration  of  the  distinctive  characteristics, 
according  to  the  degree  of  valvular  incompetency.  With  failing  compensation, 
the  secondary  curves  in  the  line  of  descent  may  disappear. 

At  the  other  end  of  the  scale  we  have  the  initial  and  sustained 
high-tension  pulses,  which  are  so  often  the  accompaniment  of  early 


Fig.  126. — Initial   High-Tension  Pulse,   from  a  Man,  Aged   Forty-eight,   with   Ar- 
teriosclerosis  and  a  Small  Aneurysm  of  the  Arch  of  the  Aorta. 

arteriosclerosis,  aneurysms  of  the  aorta,  and  chronic  interstitial 
nephritis,  typical  tracings  of  which  are  given  (Figs.  126  and 
12Y). 


Fig.  127. — Sustained   High-Tension  Pulse   from   a  Woman,  Aged    Sixty-three,  with 
Chronic  Interstitial  Nephritis. 

The  following  sphygmogram  (Fig.  128)  may  be  considered  as 
fairly  representing  the  average  in  chronic  interstitial  nephritis, 
and  is  typical  of  those  oftenest  encountered  in  this  affection. 

In  this  connection  it  is  fair  for  me  to  state  that,  highly  as  I  value  the 
sphygmograph,  it  is  my  opinion  that  its  tracings  in  chronic  interstitial  nephritis 
have  been  accorded,  in  some  quarters,  a  diagnostic  value  altogether  beyond 
their  merits.     This  is  not  to  the  discredit  of  the  instrument,  for  it  afiords  the 


822 


DISEASES   OF   THE   HEART 


best  practicable  means  for  quickly  and  conveniently  estirnating  and  permanently 
recording  the  state  of  the  circulation,  cardiac  energy,  peripheral  resistance, 
arterial  resilience,  and  arterial  tension.  On  the  contrary,  this  fictitious  value 
usually  depends  upon  a  faulty  appreciation  of  the  infinite  variations  of  the 
pulse  in  health  and  disease,  and  in  the  same  person  at  different  times. 


Fio.  128. — Fkom  a  Man,  Aued  Fuktv-five,  with  Ciiitoxic  Intekstitial  Nephritis. 

The  rhythm  of  the  pulse  is  very  clearly  and  only  satisfactorily 
shown  by  the  sphygmograph.  In  health,  the  rhythm,  in  every  par- 
ticular, is  fairly  but  not  absolutely  regular.  A  moment's  reflec- 
tion upon  the  ])liysiology  of  the  cardiac  cycle  and  the  vaso-motor 
mechanism  should  lead  us  to  expect  this,  and  an  inspection  of  any 


Fifi.  129. — FuoM  a  Woman,  Aged  Foirrv-Foin,  with  Milu  Myxcepema. 

large  collection  of  sphygmograms  will  confirm  the  inference. 
Nevertheless,  in  ordinary  health,  the  points  of  difference  between 
the  individual  pulsations  are  minute  and  well  within  the  limits 
of  physiological  identity.  However,  in  certain  conditions,  some 
of  which  are  understood  while  others  are  not,  the  pulse  becomes 


Fio.  13IJ.— I'Jiu.M 


Man,    Aoed    Twkniv-i'ih  i:,    with     VVell-Cumpen8ateu    Mitual    In- 

SUFKKJIENCY. 


decidedly  and  morbidly  irregular — arrhythmic.  These  irregu- 
larities may  be  of  almost  every  conceivable  degree  and  character, 
some  of  which  are  strikingly  peculiar. 

Tims  Ibcre  may  be  a  marked   iucciiiiility   in  the  interval  be- 
tween some  of  the  pulsations,  as  shown  in  Fig.  129,  or  beats  may 


THE  SPHYGMOaRAPH 


823 


be  entirely  lost,  as  seen  in  Fig.  130.  It  will  be  found  that  nnder 
these  circumstances  the  line  of  descent  reaches  a  lower  level  than 
it  does  in  the  regular  pulsations,  because  the  artery  has  had  a 
longer  time  in  which  to  empty  itself  through  its  distributing  chan- 
nels. In  some  cases  the  pulsation  is  not  entirely  lost,  one  or  more 
abortive  beats  showing  in  the  line  of  descent,  as  illustrated  in  Figs. 
131  and  132.  Such  pulses  are  denominated  bigeminal,  trigemi- 
nal, etc.     It  is  to  be  noted  that  the  elevation  that  marks  the  abor- 


FiG.  131. — Fhum   a    Woman,    Aged    Sixty-seven,    with    Akteriosclerosis    and    fairly 
Well-Compensated  Mitral  Incompetence. 

tive  pulsation  in  the  bigeminal  pulse  is  located  nearer  the  pre- 
ceding than  the  following  full  beat,  and  that  the  second  abortive 
pulsation  in  the  trigeminal  pulse  lies  nearer  the  first  abortive  beat 
than  does  the  latter  to  the  preceding  full  stroke. 

The  arrhythmias  thus  far  mentioned  may  be  irregular  in  their 
occurrence,  or  the  prolonged,  missed,  or  abortive  pulsations  may 
be  repeated  at  regular  intervals.  The  irregularities  of  this  group 
may  be  found  rarely  in  apparent  health,  and  frequently  in  patients 


Fig.  132. — From  a  Woman,  Aged  Seventy-three,  with  Arterioscleeosis,  and  Mitral 

Insufficiency,  Failing  Compensation. 

suffering  from  digestive  disturbances,  various  intoxications — as, 
6.  g.,  tobacco,  renal  insufficiency,  organic  disease  of  the  central 
nervous  system,  the  vagus  and  the  cardiac  ganglia,  arteriosclerosis 
of  the  coronary  arteries,  myocardial  changes,  etc.  They  occur, 
therefore,  in  conditions  of  no,  or  varying  degrees  of  danger.  They 
often  lead  to  the  discovery  of  conditions  which  without  such  warn- 
ing might  be  overlooked.  They  may,  by  the  strain  thrown  upon 
the  ventricular  walls,  lead  to  dilatation,  and  relative  valvular  in- 


824  DISEASES  OF  THE   HEART 

competence  and  thns  become  an  element  of  danger.     As  a  matter 
of  fact,  however,  many  persons  pass  throngh  the  greater  portion 


Fig.  133. — Fitosi  a  Man,  Aged  Seventy-three,  with  Artekiosclerosis,  Chronic  In- 
terstitial Nephritis,  and  Mitral  Insufficiency,  with  Failing  Compensation. 
Cheyne-Stokes  Kesvikation. 

of  a  long  life  with  such  irregularities  and  without  any  inconveni- 
ence whatever. 

In  addition  to  the  above  arrhythmias  we  have  another  group 


Fig.  134. — From  a  Woman,  Aged   Sixty-two,  with  Mitral  Obstruction  and  Eeguroi- 
TATioN,  WITH  Failing  Compensation.     Irregularly  Recurring  Delirium  Cordis. 

in  which  the  irregularities  of  the  pulse,  as  shown  by  tracings,  abso- 
lutely defy  either  analysis  or  description.     Such  pulses  are  simply 


Fig.  135. — From  a  Man,  Aged  Fifty,  with  Mitral  Keguroitation,  Lost  Compensa- 
tion, Relative  Tricuspid  Insufficiency,  Ascites,  and  (Edema  of  Legs.  Later 
Comparative  Recovery  with  Good  Compensation. 

irregularly  arrhythmic,  and  are  endless  in  their  variety,  as  may 
be  seen  in  the  few  examples  shown  (Figs.  133,  134,  135,  and  136). 


Fio.  136. — From  a  "Woman,  Aged  Tiiirty-ekiHT,  with  Mitral  Obstruction  and  In- 
sufficiency, Lost  Compensatujn,  and  Uklative  Incompetence  of  the  Tricuspid. 
Delirium  Cordis. 


THE   SPHYGMOGRAPH  825 

This  form  of  arrhythmia  is  met  with,  particularly,  in  mitral 
stenosis  and  incompetence,  arid  in  myocardial  insufficiency.  It 
is  often  a  late  plienonienon  in  mitral  disease.  It  is  of  grave,  but 
not  necessarily  of  fatal  import,  as  the  lost  compensation  may  be 
restored,  or  the  weakened  myocardium  may  regain  its  tone. 


Fig.  137. — From  a  Boy,  Aged  Twelve,  with  a  Pkeviously  Normal  Pulse,  Ten  Days 
III   with   Acute   Kheumatism,  and    on  the   Second   Day    of   Endocakditis.     No 

Murmur. 

In  endocarditis  the  sphygmograph  usually  furnishes  us  Avith 
diagnostic  evidence  of  valvular  involvement  several  hours  or  days 
before  murmurs  can  be  heard  with  the  stethoscope.    This  evidence 


Fig.   138. — From   the    Same    Patient,    Two   Years   Later,    with    Developed    Aortic 

Stenosis.     (Convalescent  from  Mumps.) 

is  shown  in  a  more  or  less  radical  change  in  the  character  of  the 
pulse,  as  shown  in  the  above  sphygmograms  (Figs.  137  and 
138). 

In  introducing  the  above  tracings  it  is  proper  for  me  to  say  that,  during 
the  past  five  years,  I  have  had  under  observation  for  one,  three,  and  five  years 
respectively,  three  cases  of  aortic  stenosis  in  young  persons,  from  each  of  whom 
tracings  of  a  similar  character  were  obtained.  In  the  slighter  cases  of  aortic 
stenosis  the  character  of  the  pulse  approximates  the  normal.  In  this  connection 
a  word  of  caution  is  due.  In  using  the  sphygmograph  in  cases  of  considerable 
or  great  aortic  obstruction  the  most  delicate  adjustment  of  the  instrument  is 
required  to  obtain  satisfactory  results.  It  may  be  said,  however,  that  the 
greater  the  care  bestowed  upon  this  point  the  more  difficult  it  will  be  to  pro- 
duce tracings  corresponding  to  some  which  have  been  made  classic  by  more 
than  a  generation's  text-book  currency. 

In  early  pulmonary  tuberculosis  the  pulse  is  often  of  a  pecul- 
iar character,  approaching,  more  or  less  closely,  the  infantile  type, 
and  the  tracings,  at  this  time,  possess  a  distinct  diagnostic  value. 
53 


826  DISEASES  OF  THE  HEART 

One  of  the  curiosities  of  clinical  spliygmography  is  the  mani- 
fest family  resemblance,  inherited  from  the  father  or  mother  by 
their  children,  often  shown  in  the  pulse  tracings. 


Fig.  139. — CAunioGiiAM  from  a  Gikl,  Ageu  Nine,  with  Mitral  Insifficiency. 

The  sphygmograph  may  be  used  to  obtain  tracings  from  the 
heart  (an  example  of  which  is  given  in  Fig.  139),  aneurysms,  pul- 
sating veins,  pulsating  tumours,  etc.,  but  the  information  to  be 
derived  from  such  tracings  is  not  very  great. 

GAERTNER'S   TONOMETER 

The  examination  of  the  circulation  includes  the  observation  of 
the  pulse  for  what  is  termed  the  arterial  or  blood  pressure.  This 
is  determined  by  heart  contraction,  the  peripheral  resistance  in 
the  arteries  and  tissues,  and  the  quantity  of  blood  contained  in  the 
vessels.  Among  skilled  physicians  there  is  often  a  difference  of 
opinion  in  regard  to  the  degree  of  the  arterial  pressure,  even  in 
general  terms,  such  as  hard  and  soft,  while  subtile  differences 
are  entirely  beyond  registration,  and,  to  most  physicians,  beyond 
perception.  Numerous  attempts  have  been  made  to  overcome  this 
difficulty  in  pulse  examinations  by  means  of  instruments;  if  suc- 
cessful, we  would  then  have  a  more  accurate  method  of  comparison 
of  the  blood-pressure  of  individuals,  and  also  of  the  blood-pressure 
of  the  same  individual  under  different  conditions.  The  invention 
of  the  sphygmograph  was  expected  to  bring  accuracy  into  the 
subject,  but  this  hope  was  not  realized.  Mosso,  von  Basch,  Iluer- 
thle,  Frey,  Oliver,  Riva-Rocci,  and  Hill  and  Barnard  may  be 
mentioned  as  inventors  of  such  instruments.  Of  these,  the  von 
Basch  instrument  was  the  most  used  up  to  1899,  since  when  the 
Gaertner  instnmient,  on  account  of  greater  simplicity  of  its  mech- 
anism, has  supplanted  it  in  the  hands  of  many,  and  has  also  intro- 
duced the  practice  of  taking  the  arterial  pressure  to  a  greater 
extent  than  had  heretofore  been  customary.  Opinions  still  vary 
as  to  the  preferable  instrument.     James  MacKenzie  (1902)  com- 


GAERTNER'S  TONOMETER  827 

pares  the  action  of  the  Hill  and  Barnard  instrument  to  that  of 
the  sphygmograph  and  regards  it  unreliable  for  blood-pressure 
registration.  So  also  with  the  Oliver  instrument.  Jarotzny  be- 
lieves the  Hill  and  Barnard  device  superior  to  those  of  von  Basch, 
Gaertner,  etc.  Ilirsch  considers  the  Gaertner  less  reliable  than 
the  von  Basch  instrument. 

As  the  latter  is  at  present  the  chief  rival  of  the  Gaertner  in- 
strument it  may  be  well  to  state  the  principle  on  which  it  works. 
There  is  a  small  compressible  rubber  pelote  connected  by  a  rubber 
tube  to  a  metallic  manometer.  By  pressure  with  the  rubber  cyl- 
inder (pelote)  a  suitable  artery  may  be  compressed  and  the 
amount  of  necessary  pressure  at  the  point  of  disappearance  or 
reappearance  of  the  pulse  on  the  peripheral  side  of  the  instrument 
is  registered  on  the  manometer.  The  radial  artery  may  be  used, 
but  the  temporals  are  usually  selected.  The  sense  of  touch  is  re- 
quired for  this  instrument,  while  in  the  Gaertner  method,  soon 
to  be  described,  sight  is  employed  for  observing  the  re-establish- 
ment of  the  circulation;  and  because  in  most  peoj^le  the  sense  of 
sight  is  more  acute  than  the  sense  of  touch,  the  Gaertner  instru- 
ment requires  less  practice  for  its  use,  and  also  is  believed  by  many 
to  be  more  accurate. 

Von  Basch  calls  his  instrument  a  sphygmomanometer.  Gaert- 
ner's  tonometer  consists  of  a  mercury  manometer,  a  rubber  bulb,  a 
"  Y  "  rubber  tubing,  and  a  small  ring  consisting  of  a  metal  frame- 
work and  encased  in  a  rubber  envelope,  which  on  inflation  stretches 
inwardly  only,  and  thus  compresses  the  finger  that  is  introduced 
into  the  ring.  These  rings  are  of  different  sizes  to  fit  large  and 
small  fingers  snugly.  One  end  of  the  "  Y  "  tube  is  attached  to  the 
manometer,  another  end  to  the  rubber  bulb,  and  the  third  end  to 
the  rubber  finger  ring;  thus  pressure  made  on  the  bulb  transfers 
itself  to  the  manometer  and  the  rubber  ring,  and  the  elastic  rubber 
on  the  inside  of  the  ring  unfolds  itself  and  makes  inward  pressure 
in  proportion  to  the  pressure  put  on  the  bulb.  The  manometer, 
being  on  the  same  closed  tubing,  registers  the  increase  or  decrease 
of  the  pressure.  A  small  clamp  is  serviceable  for  compressing  the 
bulb  firmly  and  steadily.  The  rubber  ring  is  pressed  over  the  first 
or  second  phalanx  of  any  finger  or  the  thumb.  It  is  to  fit  loosely, 
and  is  not  to  rest  on  a  joint.  An  ordinary  small  rubber  elastic  is 
now  rolled  from  the  tip  of  finger  to  the  rubber  ring.    This  produces 


82S  DISEASES   OF  THE   HEART 

an  aiui'inia  of  the  finger.  Pressure  is  now  put  on  the  rubber  bnlb 
to  a  degree  that  is  regarded  sufficient  to  nuiintain  the  anfcmia. 
This  is  usually  180  to  200  millimetres  of  the  mercury  manometer. 
The  rubber  elastic  is  now  pulled  off  the  finger,  after  which  the 
anaemic  appearance  continues  on  account  of  the  constriction  of  the 
ring.  The  pressure  on  the  rubber  bulb  is  now  gradually  lessened, 
5  millimetres  at  a  time.  After  each  diminution,  the  finger  is  ob- 
served for  a  few  seconds.  Wheii  the  pressure  is  sufficiently  lowered 
for  the  arterial  pressure  to  force  the  blood  through  thx?  arterioles 
compressed  by  the  rubber  ring,  the  anaemic  finger  first  shows  a  few 
spots  of  purple  congestion,  and  after  a  little  more  reduction  of  the 
pressure  on  the  bulb,  the  finger  becomes  entirely  suffused  with  the 
purple  colour  of  congestion,  showing  that  the  circulation  is  re- 
established. At  this  point  the  height  of  the  mercury  column  is 
observed  on  the  scale  of  the  manometer.  This  is  the  arterial  pres- 
sure expressed  in  millimetres  of  mercury. 

One  of  the  principal  objections  is  the  small  size  of  the  arteries 
utilized,  but  Gaertncr  and  others  state  that  the  pressure  in  the 
digital  arteries  is  the  lateral  pressure  in  the  volar  arch,  and  that 
this  is  probably  only  8  or  10  millimetres  lower  than  the  pressure  in 
the  radial  arteries.  Another  objection  is  that  such  small  peripheral 
arteries  are  more  under  the  influence  of  the  vaso-motor  variations 
than  large  vessels,  and  especially  subject  to  local  influences.  Cold 
anaemic  fingers  sometimes  must  be  immersed  in  warm  water  before 
the  test  can  be  made. 

It  is  well  to  follow  his  instructions  for  the  use  of  the  instrument 
very  closely.  The  individual  may  be  in  the  horizontal  or  upright 
posture.  In  the  former  the  pressure  is  a  few  millimetres  lower 
than  when  the  person  is  erect.  The  manometer  must  be  on  a  level 
with  the  heart.  A  difference  of  10  centimetres  in  the  levels  of  the 
heart  and  manometer  ])roduces  a  change  of  7  millimetres  in  the 
mercury  accordingly.  The  individual  is  to  breathe  regularly.  A 
cough  renders  the  result  unreliable  on  account  of  the  sudden  in- 
crease of  the  blood-pressure.  The  test  is  not  to  be  repeated  on 
the  same  finger  immediately  on  account  of  a  possible  persistence  of 
an  arterial  s])asm.  Thirty  seconds  will  suffice  for  a  test.  There  is 
no  pain,  but  at  the  time  of  the  re-estal)lishm(Mit  of  the  circulation 
the  person  feels  a  throbbing  and  tingling  in  the  finger. 

For  portability  a  metallic  manometer  may  be  used;  but  it  18  iiot 


GAERTNER'S  TONOMETER  829 

as  reliable;  it  should  be  frequently  compared  with  the  mercury 
manometer.  The  advocates  of  the  von  Basch  method  admit  the 
requirement  of  much  more  experience  and  careful  manipulation 
in  its  use  than  in  that  of  the  Gaertner.  The  values  obtained  by 
both  instruments  agree  fairly,  those  of  the  von  Basch  instrument 
are  probably  8  to  10  millimetres  higher ;  the  range  of  normal 
blood-pressure  under  ordinary  conditions  is  from  100  to  160  milli- 
metres of  mercury.  These  limits  may  be  narrowed  down  to  110 
to  135  for  the  greater  number  of  persons.  Constant  pressure  of 
150  to  160  should  be  regarded  suspiciously  high.  It  is  probable 
that  each  organism  has  a  mean  arterial  pressure  towards  ivhose 
maintenance  the  regulatory  mecJianism  tenaciously  strives  as  soon 
as  a  disturbance  occurs.  Active  influences  are  numerous.  For 
instance :  Posture,  food,  sleep,  physical  and  mental  work,  psychical 
conditions.  Several  readings  should  be  obtained  and  the  average 
taken ;  according  to  some  authorities  the  lowest  reading  is  the 
correct  blood-pressure,  as  more  causes  are  active  in  increasing 
than  lowering  the  blood-pressure.  According  to  Jellinek  the  ar- 
terial pressure  in  the  fingers  of  the  right  side  is  usually  slightly 
higher  than  on  the  left,  but  Eckart  and  Hirsch,  using  von  Basch's 
sphygmomanometer,  found  the  pressure  usually  higher  in  the  left 
temporal  arteries,  and  ascribed  this  to  the  direct  origin  of  the  left 
carotid  artery  from  the  aorta.  Hirsch,  who  prefers  von  Basch's 
sphygmomanometer,  maintains  that  the  Gaertner  instrument  reg- 
isters the  blood-pressure  10  to  20  millimetres  higher  than  the  von 
Basch  instrument,  but  admits  that  in  general  the  values  obtained 
by  both  instruments  agree  as  to  being  high,  medium,  or  low. 

The  high  pressures  are  of  special  interest  on  account  of  being 
associated  with  diseases  in  which  many  of  the  threatening  symp- 
toms are  thought  to  be  due  to  the  high  pressure ;  thus  in  uriemia 
and  arteriosclerosis  pressures  of  170  to  240  or  more  millimetres 
are  the  rule.  All  observers  state  that  high  pressures  are  frecjuently 
found  in  spite  of  an  apparently  soft  pulse  by  palpation;  here,  then, 
as  the  general  accuracy  of  these  instruments  cannot  be  doubted, 
their  value  is  undeniable.  In  many  illy  defined  conditions  of  mid- 
dle age  an  unusually  high  pressure  is  found,  which  returns  within 
the  normal  limits  in  the  course  of  treatment.  Such  cases  are  often 
described  as  due  to  arteriosclerosis  or  to  some  intoxication  produc- 
ing increased  arterial  pressure.     In  the  treatment  of  nej)hritis  a 


830  DISEASES   OF   THE   HEART 

lowering  of  the  arttn-ial  pressure  is  associate<l  with  improvement 
of  the  subjective  symptoms.  In  advanced  cases  of  nephritis  a  sink- 
ing of  the  blood-pressure  is  considered  to  presage  fatal  termination. 
The  influence  of  muscular  efforts  on  arterial  pressure  has  always 
been  a  mooted  point.  Both  moderate  increase  and  decrease  have 
been  claimed.  This  is  possibly  explained  best  according  to  Schott, 
who  finds  in  such  muscular  exertions,  as  wrestling,  at  first  a  slight 
increase  of  10  millimetres,  but  after  prolonged  dyspnoea  a  lowering 
of  the  pressure  from  10  to  25  millimetres.  There  is  certainly  not 
an  increase  in  the  pressure  directly  relative  to  the  amount  of 
muscular  exertion  (Kornfeld).  A  cold  bath  in  health  as  well 
as  in  fever  increases  the  blood-pressure  from  10  to  15  millimetres. 
A  bath  at  104°  reduces  the  pressure  slightl}^;  so  also  do  hot  air 
and  electric  light  sweat  baths.  Exceptions  are  occasionally  found. 
There  is  an  increase  with  digitalis,  ether,  and"  camphor,  but  this  is 
less  marked,  and  very  frequently  absent  in  fever.  In  fever  the 
cold  bath  alone  may  be  relied  upon  to  increase  the  pressure  (Mer- 
candino  with  the  Riva-Rocci  instrument)  ;  psychic  excitement 
regularly  increases  the  blood-pressure  from  10  to  20  millimetres, 
hence  first  examinations  often  are  too  high.  In  neurasthenia  an 
increase  of  10  to  20  millimetres  is  so  common  that  Federn,  Kraus, 
and  Ileim  regard  it  a  sign  of  diagnostic  value,  especially  in  chil- 
dren. In  hfcmatemesis  and  haemoptysis  there  occurs  a  slight  in- 
crease of  arterial  pressure  on  the  second  and  third  days ;  in  acute 
fevers  there  is  sometimes  a  slight  rise,  sometimes  a  slight  sinking 
of  the  blood-pressure.  The  fever  does  not  seem  to  have  a  constant 
influence,  but,  rather,  the  blood-pressure  varies  on  account  of  other 
factors  occurring  in  the  course  of  the  fever.  For  phthisis  a  constant 
low  pressure  indicates  progression,  but  in  the  early  stages  there  is 
usually  little  change;  as  the  disease  progresses  the  pressure  sinks 
on  account  of  the  diminution  in  tlie  ])eriplieral  resistance  (Burck- 
hardt-lfensen).  There  is  a  diminution  in  anicmia,  cachexia,  sleep, 
and  acute  cardiac  weakness.  A  pressure  of  GO  millimetres  is  con- 
sidered very  grave. 

Gaertner  states  that  his  instrument  registers  mean  and  not 
maximal  pressure.  This  is  not  accepted  by  all.  However  this 
may  be,  we  must  remember  that  the  actual  blood-pressure  can  be 
obtained  only  by  the  introduction  of  a  cannula  into  an  artery,  as 
has  been  done  in  the  course  of  operations  by  Albert,  who  found  the 


THE  SPHYGMOMANOMETER  831 

pressure  to  be  in  tlic  anterior  tibial  artery  between  100  and  100 
millimetres  of  mercury;  Kiihe-Wiegand  during  ura-mia,  155  mil- 
limetres in  a  radial  artery ;  Faiore  in  the  femoral  and  brachial 
arteries,  120  and  110  millimetres;  but  such  direct  methods  are 
out  of  the  question  for  ordinary  clinical  purposes.  The  Gaertner 
instrument,  as  well  as  all  the  other  instruments,  are  influenced 
by  the  resistance  of  the  tissue  of  the  artery  and  the  surrounding 
structures.  Von  Baseh  estimates  that  the  resistance  of  an  empty 
temporal  artery  to  compression  is  1  millimetre  and  that  of  an  ather- 
omatous artery  5  millimetres.  The  resistance  of  the  soft  tissues 
over  the  temporal  artery  is  about  6  to  8  millimetres.  So  after  all 
we  are  not  dealing  with  figures  of  the  actual  pressure  within  the 
artery,  but  with  relative  figures.  If  all  precautions  are  observed, 
these  figures  may  surely  be  used  for  comparisons  of  blood-pressure 
changes  in  the  same  individual  with  a  great  degi-ee  of  reliability; 
while  in  comparisons  among  different  individuals  much  more  cau- 
tion must  be  observed.  Although  no  defined  clinical  value  can  as 
j'et  be  claimed  for  these  researches  except  in  diseases  of  liigh  arte- 
rial pressure,  the  necessity  for  more  attention  to  arterial  pressure 
has  become  very  apparent  within  the  last  ten  years,  as  shown  by 
numerous  articles  appearing  on  this  subject,  especially  in  Ger- 
many; and  since  there  are  now  several  instruments  giving  prac- 
tical results,  we  may  hope  that  soon  a  clearer  understanding  of  the 
blood-pressure  problems  will  be  forthcoming,  especially  in  cardiac 
diseases  and  acute  fevers,  so  that  both  diagiiosis  and  therapeutic 
indications  will  become  more  accurate  than  has  thus  far  been  pos- 
sible, even  with  the  acumen  of  the  most  experienced. 

THE  SPHYGMOMANOMETER 

Since  the  foregoing  excellent  presentation  of  the  advantages 
to  be  gained  from  the  clinical  use  of  sphygmomanometry  and  of 
the  application  to  this  end  of  the  Gaertner  tonometer  was  written 
by  Dr.  Otto  Schmidt,  the  employment  of  some  form  of  blood- 
pressure  apparatus  has  become  general  among  clinicians,  thus  ful- 
filling the  prediction  expressed  in  his  closing  paragTaph.  More- 
over, in  1904  appeared  an  excellent  work  on  "  The  Clinical  Study 
of  Blood-pressure  "  by  Theodore  C.  Janeway  which  gave  impetus 
to  the  adoption  by  physicians  of  this  indispensable  aid  to  diag- 


832  DISEASES  OF  THE  HEART 

nosis;  so  that  now  no  up-to-date  physician  or  hospital  is  without 
some  form  of  sphygmomanometer. 

The  Gaertner  instrument  is  not  in  wide  use  for  a  number  of 
reasons.  In  the  first  place  it  was  found  necessary  to  have  a  large 
assortment  of  finger  rings  of  different  sizes  in  order  to  obtain 
trustworthy  results.  Also  the  instrument  recorded  only  maximal 
pressures,  and  lastly  it  was  considered  by  many  not  desirable  to 
measure  the  pressure  in  arteries  of  such  small  calibre  as  in  the 
terminal  phalanx  of  a  finger. 

Accordingly,  the  sphygmomanometers  now  meeting  with  great- 
est favour  in  the  United  States  for  general  use  at  the  bedside  are 
such  as  are  modeled  after  the  Riva-Rocci  instrument.  In  other 
words,  practically  all  the  sphygmomanometers  now  employed  pro- 
duce compression  of  the  brachial  artery  by  means  of  an  arm-band 
of  rubber  which  can  be  inflated  with  air  so  as  to  shut  off  the 
supply  of  blood  to  the  radial,  the  vessel  selected  for  palpation  by 
the  operator.  By  means  of  a  Y-shaped  tube  the  arm-band  is  con- 
nected with  a  mercurial  manometer  as  well  as  with  the  inflating 
bulb,  and  thus  the  amount  of  blood-pressure  required  to  overcome 
the  constriction  of  the  arm-band  is  shown  in  millimetres  by  the 
manouicter. 

The  only  essential  differences  in  the  various  sphygmouianome- 
ters  of  this  type  consist  in  the  width  of  the  arm-band  and  of  the 
mercurial  manometer.  The  Riva-Iiocci  is  relatively  narrow  in 
both  these  respects,  and  as  higher  readings  are  obtained  when  the 
compressing  armlet  is  narrow,  it  is  thought  preferable  to  have  an 
arm-band  of  10  cm.  to  12  cm.  in  width.  Moreover,  as  a  manome- 
ter of  small  calibn;  does  not  show  ])lainly  the  fluetuatious  in  the 
mercurial  colunm  by  which  the  diastolic  blood-pressure  is  deter- 
mined, and  as  it  is  desirable  to  ascertain  both  diastolic  and  systolic 
pressures,  the  Stanton,  the  Janeway  and  some  others  are  provided 
with  relatively  wide  manometers.  In  addition  to  these  advan- 
tages tliey  can  be  carried  about  with  comparative  ease,  and  are 
thus  available  at  the  bedside  as  well  as  in  the  office. 

The  Erlanger  instrument  is  ])('r]ia]is  the  most  exact  of  any, 
since  it  enables  one  to  obtain  a  graphic  record  besides  showing 
both  systolic  and  diastolic  pressures,  and  for  hospital  and  lal)ora- 
tory  use  cannot  be  excelled.  It  is  both  expensive  and  complicated 
and  rather   too  cumbersome   for  ready   portability.      It  may  be 


THE  SPHYGMOMANOMETER  833 

stated  parenthetically  tlial;  Hirschfelder  has  devised  an  attach- 
ment to  Erlanger's  sphygmomanometer  which  converts  it  into  a 
polygraph  as  well.  So  that  the  apparatus  is  availahle  for  record- 
ing the  characters  of  jugular  pulsations  as  well  as  blood-pressure. 

The  method  of  use  of  the  ordinary  sphygmomanometers  is  very 
simple  and  requires  only  practice  to  admit  of  trustworthy  results. 
For  the  sake  of  readers  who  ma}^  not  be  familiar  Avith  these  in- 
struments, the  mode  of  application  will  be  briefly  described.  The 
arm-band  is  fastened  snugly  but  not  tightly  about  the  arm  midway 
l)etwcen  shoulder-joint  and  elbow,  care  being  taken  that  the  man- 
ometer be  on  a  level  with  the  heart,  whether  the  patient  be  sitting 
or  reclining.  The  physician,  having  assured  himself  tliat  the  vari- 
ous connections  are  perfect  and  the  manometer  free  from  air,  now 
inflates  the  armlet  until  his  finger,  resting  on  the  radial  artery, 
perceives  that  the  pulse  is  totally  obliterated.  Then  allowing  the 
air  to  escape  gradually  from  the  arm-band  or  cuff  so  that  the 
mercurial  column  falls  a  few  mm.  at  a  time,  he  watches  atten- 
tively for  the  instant  when  his  palpating  finger  appreciates  the 
first  tiny  flickering  of  the  returning  pulse-wave.  With  his  eye 
on  the  manometer  he  reads  the  number  of  mm.  recorded  at  that 
instant.  This  done,  he  may  again  obliterate  the  pulse  and  repeat 
in  order  to  verify  his  first  reading.  This  gives  him  the  systolic 
blood-pressure.  Thereupon  he  permits  the  column  of  mercury  to 
sink  5  mm.  at  a  time  until  at  length  the  lowest  point  is  reached 
at  which  the  mercury  still  oscillates  the  most  widely.  This  so- 
called  maximal  pulsation  gives  the  diastolic  pressure,  and  the  point 
midway  between  the  systolic  and  diastolic  pressure  is  the  mean 
pulse  pressure  for  that  particular  case. 

According  to  Janeway  and  others  the  upper  limit  of  normal 
systolic  pressure  may  be  set  at  145  mm.  with  a  12  cm.  arm-band, 
with  a  Itiva-Eocci  10  to  15  mm.  higher.  The  minimum  normal 
pressure  for  an  adult  is  100  mm.,  or  possibly  90  mm.,  with  a 
wide  armlet,  l^eing  with  a  narrow  band  correspondingly  higher. 
In  healthy  young  men  the  systolic  pressure  may  be  put  down  as 
from  100  to  130  mm.,  while  in  females  it  is  perhaps  10  mm. 
lower. 

In  children  under  two  years  Janeway  believes  the  pressures 
are  undoubtedly  still  lower,  from  75  to  90  mm.  being  usual.  In 
older  children  the  figures  correspond  to  the  lower  values  in  adults 


834  DISEASES  OF  THE   HEART 

(90  to  110  mm.),  am!  the  difference  between  the  systolic  and 
diastolic  is  smaller.  In  elderly  individuals  the  systolic  pressures 
obtained  are  generally  higher,  but  since  in  some  aged  persons  rela- 
tively low  readings  may  be  obtained,  the  likelihood  is  that  high 
figures  Avhen  not  so  high  as  to  come  within  the  limit  of  patholog- 
ical hypertension  are  owing  to  stiffness  of  the  vascular  coats  and 
to  obesity,  in  consequence  of  which  latter  more  air-pressure  in  the 
arm-band  is  required  to  obliterate  the  pulse. 

The  normal  diastolic  pressure  in  any  given  case  Janeway  be- 
lieves to  be  from  25  to  40  mm.  below  the  systolic  in  the  same 
person.  This  holds  true  only  during  rest,  as  do  tlie  systolic  pres- 
sures given  above.  Accordingly,  the  normal  range  of  diastolic 
blood-pressure  may  be  given  as  between  G5  and,  110  mm.  The 
conditions  which  tend  to  increase  systolic  pressure,  especially  the 
pathological  ones,  seem  to  exert  less  influence  upon  the  diastolic 
and  therefore,  this  taken  indei)endently  of  the  systolic,  is  not  a 
trustworthy  index  of  the  actual  state  of  blood-pressure. 

The  many  different  factors  influencing  blood-pressure  are  not 
satisfactorily  established,  but  the  following  precautions  based  on 
such  facts  as  are  known  may  be  laid  down  as  essential  in  esti- 
mating the  significance  of  clinical  readings.  Mental  and  emo- 
tional excitement  raise  the  systolic  pressure,  and  hence  if  the 
patient  is  much  perturbed  by  the  examination  the  observation 
should  be  postponed  until  all  excitement  has  passed  or  the  record 
should  be  checked  by  observations  made  on  other  days  under  as 
nearly  all  other  similar  conditions  as  possible.  All  readings  in  the 
case  of  any  one  individual  should  be  taken  in  the  same  posture, 
sittiiig  or  reclining,  but  preferably  the  latter  since  it  conduces  to 
greater  ease  of  body  and  perhaps  of  mind.  Since  there  are  diurnal 
variaticms  in  the  systolic  blood-pressure,  it  is  best  to  make  sphyg- 
momanometric  records  at  the  same  hour  of  the  day  in  each  case. 
The  instrument  should  be  so  placed  as  to  stand  on  a  level  with  the 
heart  to  overcome  the  force  of  gravity.  If  possible,  the  physician 
should  never  content  himself  with  a  single  observation,  but  should 
verify  the  results  first  obtained  by  readings  made  on  subsequent 
occasions. 

Since  permanent  hypertension  of  the  arterial  pulse  is  to  be 
regarded  as  pathological  it  interests  every  i)ractitioner  to  know 
what  he  may  interpret  as  falling  within  the  bounds  of  hypertcn- 


THE   SPTIYO:\K):\rANOMETER  835 

sion.  Accordingly,  the  fig^iires  given  by  -laneway  may  liere  be 
stated.  In  a  young  person  any  pi-essiire  above  135  nnn.  (12  cm. 
arm-band)  may  be  regarded  with  sns2)icion.  In  an  older  one  145 
mm.  (broad  armlet)  and  above  145  mm.  in  an  individual  before 
middle  age  or  160  mm.  after  middle  age  are  definitely  patholog- 
ical if  repeatedly  present  as  the  average  reading.  The  lowest 
normal  pressure  in  adults  may  be  given  as  90  mm.,  in  children 
as  80  mm.  If  a  5  cm.  arm-band  is  used,  the  readings  are  all  from 
15  to  20  mm.  higher. 

Finally^  the  query  of  practical  importance  is  in  what  class  of 
cases  is  one  to  look  for  abnormally  high  blood-pressure.  Concisely 
it  may  be  stated  that  persistent  blood-jjressure  above  normal  limits 
should  put  the  physician  on  his  guard  and  cause  him  to  look  with 
suspicion  upon  the  state  of  the  kidneys,  the  vascular  system  and 
the  heart  muscle.  It  is  the  detection  of  arterial  hypertension  which 
many  times  enables  one  'to  estimate  correctly  changes  in  urine  and 
heart  findings  which  otherwise  might  be  thought  insignificant. 
Strangely  enough,  however,  it  is  to  be  remembered  that  the  blood- 
pressure  is  not  invariably  too  high  in  persons  whose  hearts,  vessels 
and  even  kidneys  are  found  on  clinical  investigation  to  exhibit 
signs  of  degeneration.  Such  seems  to  be  the  case  particularly  in 
pronounced  arterio-sclerosis.  In  cases  plainly  of  chronic  nephritis 
the  blood-pressure  is  with  but  few  exceptions  far  above  the  normal 
so  long  as  the  heart  is  adequate.  As  the  myocardium  fails  in  its 
sufficiency  blood-pressure  falls,  and  hence  a  marked  and  persistent 
sinking  of  the  pulse  tension  is  an  omen  of  grave  danger.  The 
same  is  true  of  a  pronounced  and  persistent  increase,  since  it  may 
portend  apoplexy,  uraemia  or  overpower  the  functional  integrity 
of  the  myocardium. 

In  valvular  diseases  the  sphyg-momanometer  is  not  of  as  great 
value,  and  yet  as  emphasized  by  Janeway  the  systolic  blood- 
pressure  may  give  us  aid  in  arriving  at  a  differential  diagnosis. 
Inasmuch  as  stenosis  of  an  ostium  lessens  the  amount  of  blood 
discharged  into  the  aorta  with  each  systole  and  also  tends  to  cause 
slowing  of  the  pulse-rate,  it  may  be  stated  that  a  persistently  low 
blood-pressure  makes  in  favor  of  narrowing  as  against  regurgi- 
tation. 

For  instance,  in  aortic  insufficiency  it  is  exceedingly  common 
to  hear  both  a  systolic  and  a  diastolic  murmur,  and  the  physician 


836  DISEASES   OF   THE   HEART 

is  sometimes  at  a  loss  to  decide  Avhether  stenosis  as  well  as  regur- 
gitation is  present.  Xow  it  is  known  that  a  powerful  left  ven- 
tricle discbarges,  when  the  leak  is  free  and  the  ostium  is  not  nar- 
rowed, a  larger  than  normal  volume  of  blood  with  great  force. 
Consequently,  as  I  have  observed  repeatedly,  the  systolic  blood- 
pressure  in  such  instances  is  high^  well  up  to  the  normal  upper 
limit  or  even  beyond.  Therefore,  if  in  a  given  case  with  a  to- 
and-fro  aortic  bruit  the  systolic  blood-pressure  is  relatively  low, 
it  makes  for  a  combined  stenosis  and  insufficiency.  This  holds 
true,  however,  only  so  long  as  compensation  is  preserved,  for  with 
failing  power  on  the  part  of  the  left  ventricle  systolic  blood-pres- 
sure tends  to  sink.  That  such  is  correct  is  proven  by  the  observa- 
tion repeatedly  made  by  me  that  with  reinstatement  of  ventricular 
energy  the  blood-pressure  has  risen  to  a  permanently  higher  level. 

In  the  same  manner,  the  state  of  systolic  blood-pressure  may  be 
utilized  within  certain  limits  in  the  determination  of  the  degree 
of  stenosis  present  at  the  mitral  orifice.  The  greater  the  narrow- 
ing, the  lower  should  be  the  systolic  pressure.  Yet  even  in  such 
a  case  the  frequency 'of  the  heart's  action  must  be  taken  into  con- 
sideration. As  a  general  proposition  it  may  be  stated  that,  given 
a  relatively  slow  pulse  in  a  case  of  mitral  stenosis,  the  pulse  pres- 
sure should  be  comparatively  low  as  contrasted  with  that  of  pre- 
dominating mitral  regurgitation.  Still  even  here  the  height  of  the 
blood-pressure  must  depend  largely  upon  the  volume  of  blood  dis- 
charged into  the  aorta  and  the  force  with  which  it  is  discharged. 

After  all,  the  sphygmomanometer  is  not  of  as  much  value  in 
the  diagnosis  of  valvular  as  of  myocardial  lesions.  It  may  give 
valuable  information,  however,  in  enabling  one  to  formulate  prog- 
nosis and  occasionally  in  deciding  ujxyu  a  line  of  treatuient.  If 
the  pressure  is  found  persistently  very  low,  and  especially  below 
normal  minimal  limits,  the  state  of  the  patient  is  grave,  since 
a  blood -pressure  of  60  mm.  is  regarded  as  close  to  the  danger 
point.  In  any  case,  therefore,  showing  low  rather  tlian  liigli  read- 
ings, the  heart  tonic  called  for,  other  things  being  equal,  is  digi- 
talis, since,  as  is  well  known,  this  remedy  tends  to  improve  vaso- 
motor tone,  and  in  valvular  lesions  a  loss  of  vascular  tonus  is  often 
a  prominent  factor  in  preventing  a  re-establishment  of  compen- 
sation. 


INDEX 


Aberrant  cords,  30. 

Abortion,  causing  acute  endocarditis, 

180. 
Adherent  pericardium,  99; 

Broadbent's  sign  in,  119; 

Friedreichs'  sign  in,  120; 

Kussmaul's  sign  in,  120. 
Adhesions,      chronic      mediastinoperi- 
eardial,  102; 

formation  of,  in  chronic  pericarditis, 
103. 
Age,   influence   of,   in   mitral   stenosis, 
254; 

in  valvular  lesions,  407. 
Air  hunger,  157. 
Alcoholism,  in  acute  endocarditis,  47 ; 

in  aortic  regurgitation,  280. 
Amyl,   nitrite   of,   in   angina   pectoi'is, 

658. 
Aneurysm,  congenital,  769; 

cases  of,  61,  746. 
Aneurysm,  of  thoracic  aorta,  775; 

associated    with    expectoration    and 
cough,  784; 

auscultation  in,  802; 

cases  of,  779,  794,  799,  804; 

diagnosis  of,  804; 

dyspnoea  in,  783; 

electrolysis  in,  811; 

etiology  of,  777; 

injection  of  gelatin  in,  787; 

of  gelatin  and  salt  solution,  812; 

inspection  in,  800; 

morbid  anatomy  of,  775; 

morphine  in,  813; 

pain  in,  782; 

palpation  in,  801 ; 

percussion  in,  802; 

physical  signs  in,  800; 

prognosis  in,  808; 

symptoms  of,  781 ; 

syphilis  in,  778; 

treatment  of,  S09; 

tuberculosis  in,  808. 
N 


Angina  pectoris,  637; 

aconite,  not  used  in,  660; 

amyl   nitrite  in,   658; 

anodynes  in,  660; 

brandy  in,  660; 

cases  of,  645,  652,  653 ; 

chloroform  and  ether  in,  658; 

diagnosis  of,  654; 

digitalis  in,  662; 

etiology  of,  640; 

nitroglycerin  in,  658; 

opium  in,  658,  659; 

pathology  of,  640; 

prognosis  in,  657 ; 

strophanthus  in,  662; 

syphilis  in,  646 ; 

treatment  of,  658. 
Angina  pseudo-pectoris,  719. 
"  Angina-sclero-tabagique,"  648. 
Anodynes,  88. 
Antistreptococcus    serum.        (See    Se- 

I'um.) 
Antitoxin,  in  acute  endocarditis,  193; 

in  acute  myocarditis,  515. 
Aorta,  stenosis  of   (see  Stenosis) ; 

thoracic,  aneurysm  of,  775. 
Aortic    regurgitation    (see    Regurgita- 
tion) ; 

stenosis   (see  Stenosis). 
Aortitis,  acute,  759; 

etiology  of,  760; 

inspection  in,  761 ; 

in  measles,  760; 

morbid  anatomy  of,  159; 

nitroglycerin  in,  762; 

palpation  in,  761; 

percussion  in,  761 ; 

physical  signs  in,  762; 

in   pneumonia,  760; 

prognosis  in,  762 ; 

in   scarlatina,   760; 

strychnine  in,  762; 

symptoms  of,  760; 

treatment  of,  762. 

837 


838 


DISEASES  OF   THE   HEART 


Apncea,  in  Cheyne-Stokes  respiration, 

615. 
Applications,  cold   (see  Ice-Bag) ; 

hot,  in  acute  endocarditis,  190, 
Area,  aortic,  25; 

cartliac,  25; 

mitral,  26; 

pulmonary,  25; 

tricuspid,  26. 
Arrhythmia,    in    chronic    endocarditis, 

214. 
Arterial  system,  diseases  of,  738. 
Arteries,  congenital  smallness  of,  773; 

diagnosis  of,  774; 

prognosis  in,  774; 

symptoms  of,  773; 

treatment  of,  774. 
Arteriosclerosis,  738; 

bronchitis,   chronic,   resulting   from, 
749; 

calomel  in,  757; 

cases  of,  746,  753; 

diagnosis  of,  751; 

digitalis  in,  757; 

etiology  of,  741 ; 

jalap  in,  757; 

morbid  anatomy  of,  739; 

nitroglycerin  in,  757 ; 

physical  signs  in,  750; 

prognosis  in,  754; 

strophanthus  in,  757; 

symptoms  of,  745; 

syphilis  in,  742. 
Arteritis,  acute,  762; 

diagnosis  of,  763; 

digitalis  in,  762; 

inspection  in,  763; 

morbid  anatomy  of,  762; 

palpation  in,  763; 

physical  signs  in,  763; 

prognosis  in,  763; 

symptoms  of,  762; 

treatment  of.  763. 
Arteritis,  syphilitic,  764; 

diagnosis  of,  766 ; 

etiology  of,  765 ; 

morbid  anatomy  of,  764; 

prognosis  in,  766; 

symptoms  of,  765; 

treatment  of,  766. 
Artery,  cerebral,  rupture  of,  in  liyp^r- 
trophy  of  left  ventricle,  574; 

pulmonary,   stenosis  of    (see   Steno- 
sis). 
Ascites,  in  adherent  pericardium,  117. 
Asthma,   cnrdinc,   237,   (U.S. 


Asthma,  bromides  in,  563; 

in  mitral  stenosis,  270. 
Atheroma.      (See  Arteriosclerosis.) 
Atrophy  of  the  heart,  667 ; 

diagnosis  of,  6(i8; 

etiology  of,  667 ; 

morbid  anatomy  of,  667; 

prognosis  in,  668; 

symptoms  of,  668; 

treatment  of,  668. 
Atropine,    in    Cheyne-Stokes    respira- 
tion, 623; 

in  valvular  lesions,  500. 
Attack,  neuroses,  treatment  of,  727. 

Bacilli.      (See   Micro-organisms.) 
Bacteria.      (See  Micro-organisms.) 
Baths,  hot,  evil  effect  of,  in  valvular 
lesions,  427. 
in  valvular  lesions,  427,  466,  503; 
Nauhcim,  110,  115,  464,  503,  592; 
saline,  in  valvular  lesions  466; 
Turkish,  552. 
Belladonna,  in  pericarditis,  88. 
Benign  endocarditis.     (See  Endocardi- 
tis.) 
Bloodletting,    in    dilatation    of    heart, 

591. 
Blue  baby,  of  congenital  heart  disease, 

692,  701. 
Bradycardia,  624; 

diseases  associated  with,  625; 
Breathing,   Cheyne-Stokes,   diseases  in 

which,  observed,  617. 
Bright's  disease,  in  pericarditis,  acute, 
45; 
chronic,    in    Cheyne-Stokes    respira- 
tion, 617; 
in  myocarditis,  chronic,  539; 
in  regurgitation,  mitral,  237. 
Broadl)enfs  sign  in  adherent  pericar- 
dium, 119. 
Bronchial    disorders,    in    valvular    le- 
sions, 407. 
Bronchitis,  in  pericarditis,  acute,  47; 
in  pericarditis,  chronic,   102. 

Caffeine,  in   tachycardia,  736: 

in  valvular  lesions,  432. 
ralcification    in    pericarditis,    chronic, 

101. 
Calomel,  in   arteriosclerosis,  757; 

in  pericarditis,  chronic,  125 ; 

with  oirusion.  89 ; 

in  valvular  lesions,  4.32,  448,  491,  493. 
Cancer,  of  the  mvocardium,  666. 


INDEX 


839 


Cardiac  asthma   (see  Asthma) ; 
neurosis,  703; 
pain,  718. 
Catarrh,   bronchial,   in   mitral   lesions, 

407. 
Cathartics,  in  dilatation,  592; 
in  endocarditis,  chronic,  202; 
in  valvular  lesions,  41)2. 
Cheyne-Stokes  respiration,  017; 
case  of,  022; 
in  diphtheria,  617; 
morphine  in,  023; 
in  pneumonia,  017; 
prognosis  in,  022; 
treatment  of,  623. 
Chills  and  fever,  in  suppurative  peri- 
carditis,  72. 
Chloralamide,  in  chronic  myocarditis, 

563. 
Chloral   hydrate,   in   valvular   lesions, 

501. 
Chloralose,  in  valvular  lesions,  501. 
Chlorosis,  in  mitral  insutficiency,  597. 
Chorea,  in  acute  endocarditis,  153,  154, 

155. 
Cirrhosis,    atrophic    hepatic,    differen- 
tiated from  adherent  pericardium, 
122; 
renal,  leading  to  tricuspid  regurgi- 
tation, 345. 
Climate,  change  of,  in  valvular  lesions, 

432. 
Clothing,  in  valvular  lesions,  425,  476. 
Codeine,  in  pericarditis,  88,  91. 
Compensation,   imperfect,  in   valvular 
lesions,  435.' 
lost,  478; 
perfect,  413,  414; 

prevented,    in    chronic    pericarditis, 
105. 
Congenital     aneurysm.       (See     Aneu- 
rysm.) 
Congenital  diseases  of  the  heart,  686; 
case  of,  698; 
diagnosis  of,  701 ; 
etiology  of,  689 ; 
inspection  in,  695; 
morbid  anatomy  of,  686; 
morphine  in,  693 ; 
palpation  in,  696. 
Congenital  smallness  of  arteries.     (See 

Arteries.) 
Congestion,  abdominal  viscera,  in  aor- 
tic and  mitral  regurgitation,  397 ; 
cerebral,    in    mitral     regurgitation, 
237. 


Congestion,   chronic   pulmonary,   231; 

venous,  397. 
Cords,  aberrant,  30. 
Corpulent,  cardiac  inadequacy  of  the, 

599. 
Cough,  in  aneurysm  of  thoracic  aorta, 

784. 
Cusp,  rupture  of,  in  aortic  regurgita- 
tion, 278. 
Cyanosis,  in   acute  endocarditis,   171; 
in  aortic  stenosis,  335; 
in  dilatation,  585; 
in  tricuspid  regurgitation,  347. 

Death,  mode  and  causes  of,  in  aneu- 
rysm of  thoracic  aorta,  808; 

in  regurgitation,  aortic,  307; 

mitral,  247; 

pulmonary,  374; 

tricuspid,   354 ; 

in  stenosis,  aortic,  340; 

mitral,  270; 

pulmonary,  388; 

tricuspid,  364; 

sudden,  in   syphilis   of  the  myocar- 
dium, 665. 
Deglutition,    painful,   in    diy   pericar- 
ditis, 49. 
Delirium,  in  mitral  stenosis,  270. 
Devices,  mechanical,  as  aids  to  deter- 
mining diseases,  815. 
Dextrocardia,   acquired,   682; 

diagnosis  of,  684; 

etiology  of,  683; 

inspection  in,  685; 

morbid  anatomy  of,  682; 

palpation  in,  684; 

percussion  in,  684; 

prognosis  in,  685 ; 

symptoms  of,  684; 

treatment  of,  685; 

tuberculosis  in,  681. 
Dextrocardia,  congenital,  681; 

case  of,  681 ; 

symptoms   of,   681. 
Diathesis,   rheumatic,   in   valvular  le- 
sions, 406. 
Digitalis  in  arteriosclerosis,  757; 

in  arteritis,  762; 

in  angina  pectoris,  662 : 

in  dilatation,  591; 

in  endocarditis,  acute,  189: 

in  endocarditis,  chroni'.    202; 

in  fatty  heart,  611; 

in  functional  disorders,  709; 

in  hypertrophy,  575. 


840 


DISEASES  OP   THE   HEART 


Digitalis  in  mitral  insiiilkioncy,  598; 

in  niyoeaiditis,  aeiito,  51(5; 

in  myocarditis,  chronic,  552,  5G4; 

in  pericarditis,  chronic,   120; 

in  pericarditis,  dry,  54; 

in  pericarditis,  with  effusion,  83; 

routine     administration,     objection- 
able, 89; 

in   pneumopericardium,    1315; 

in  regurgitation,  aortic,  2S8,  290; 

in  regurgitation,  mitral,  225; 

in  stenosis,  aortic,  326; 

in  stenosis,  mitral,  272; 

in  stenosis,  tricuspid,  359; 

in  Stokes-Adams  disease,  G36; 

in  syphilis,  of  myocardium,  GG5; 

in  tachycardia,   73G; 

in  valvular  lesions,  394,  430,  480; 

warning  in  regard  to  use  of,  497. 
Dilatation,  57G; 

baths  in,  592; 

bloodletting  in,  591 ; 

blue  mass  in,  591 ; 

eases  of,  582,  584,  593; 

cathartics  in,  592; 

cyanosis  in,  584; 

diagnosis  of,  58G; 

digitalis  in,  591; 

etiology  of,  577; 

influenza  in,  577; 

inspection  in,  585; 

morbid  anatomy  of,  57G; 

morphine  in,  593; 

nitroglycerin  in,  591,  593; 

palpation  in,  585; 

percussion  in,  585; 

phj'sical  signs  in,  585; 

prognosis  in,  587 ; 

resistance  exercises  in,  592; 

rheumatism  in,  401,  429; 

secondary  to  pericarditis,  101 ; 

strychnine  in,  591 ; 

symptoms  of,  580; 

treatment  of,  590. 
Diphtheria,  in  bradycardia,  625; 

in  Cheyne-Stokes  respiration,  017; 

in  endocarditis,  acute,  156; 

in  myocarditis,  acute,  508,  511; 

in  pericarditis,  acute,  46; 

in  tachycardia,  732. 
Diphtheritic  endocarditis.      (See  Endo- 
carditis.) 
Disorders,  funcfional.      (See  Function- 
al Disorders.) 
Dropsy,  in  hydropericardium,  130; 

in  myocarditis,  chronic,  530,  .563. 


Dropsy,  in  regurgitation,  mitral,  219, 
236,  245; 
cause  of,  in  tricuspid  regurgitation, 

348; 
in  regurgitation,  tricuspid,  351; 
in  valvular  lesions,  470. 
Drugs,  use  of,  in  valvular  lesions,  430. 
Duroziez's    sign,    in    aortic   regurgita- 
tion, 305. 
Dyspepsia,  chronic,  in  bradycardia,  G25. 
Dyspnoea,  in  aneurysm,  aortic,  783; 
in  endocarditis,  acute,  171; 
in  regurgitation,  mitral,  238; 
in  stenosis,  mitral,  257. 

Electrolysis,  in  aneurysm   of  thoracic 

aorta,  811. 
Embolism,    septic,    in    acute    endocar- 
ditis, 158,   172,   184. 
Emphysema,  in  hypertrophy,  570. 
Endarteritis  obliterans,  766; 

diagnosis  of,  768; 

etiology  of,  767; 

morbid  anatomy  of,  766; 

prognosis  in,  768; 

symptoms  of,  767; 

treatment  of,  769. 
l']ndocarditis,   acute,    143; 

abscess  in,  156,  181 ; 

aconite,  not  used  in,  189; 

alcohol  in,  192; 

alkalies  in,  187; 

api)lica1ions  in,  hot,   190; 

associated  with  myocarditis,   157; 

associated  with  pericarditis,  101,157; 

bacillus  of  diphtheria   in,   151,   156; 

of  influenza  in,  151,  156; 

of  typhoid  fever  in,  151 ; 

bacteria,  pyogenic,  in,   149,  150; 

blister  in,  isS; 

brandy  in,  191 ; 

bromides  in,  189; 

camphor  in,   191 ; 

in  cancer,  156; 

cases  of,  158,  164,  170; 

chorea  in,  1,53,  1.54,  155; 

cour.se  of,  163; 

cyanosis  in,  171 ; 

diagnosis  of,   163; 

diagnosis,  differential,  from  typhoid 
fever,  182; 

digitalis  in,  189; 

dyspud-a  in,  171; 

emboli  in,  172; 

ether  in,  191; 

etiology  of,   143. 


INDEX 


8il 


Endocarditis,     acute,     hemiplegia    in, 

158,    184; 

ice-bag  in,  18!); 

indicated  by  rlieunialic  fever,  157; 

infarction  in,  158; 

in  foital  life,  143; 

inspection  in,  17G; 

leucocytosis  in,   181 ; 

in  measles,  154; 

morbid  anatomy  of,  143; 

mori)liine   in,    175; 

opium  in,  190; 

oxygen  in,  191 ; 

palpation  in,   176; 

in  pelvic  disease,  155; 

percussion  in,  177; 

physical  signs  in,  176;    , 

in  pneumonia,   ISG; 

in  pyaemia,  156; 

pyrexia  in,  171 ; 

resulting  from  enteric  fever,  154; 

resulting  from  gall-stones,  156; 

resulting  from  scarlet  fever,  154; 

rheumatism   in,    146,   152,   153,   157, 
181,  186,  187; 

sepsis  in,  170,  193; 

serum,  antistreptocoeeus  in,  193; 

in  small-pox,  154; 

strophanthus  in,   169; 

strychnine  in,  169,  191 ; 

symptoms  of,   157 ; 

in  tonsillitis,  156; 

treatment  of,   187. 
Endocarditis,  benign,  143. 
Endocarditis,  chronic,  199; 

arrhythmia  in,  214; 

cases  of,  201,  206,  210; 

cathartics  in,  202; 

digitalis  in,  202; 

etiology  of,  201 ; 

morbid  anatomy  of,   199; 

nitroglycerin  in,  202; 

rheumatism  in,  204; 

strychnine  in,  202; 
symptoms   of,   205; 

syphilis  in,  204; 

treatment  of,  202. 
Endocarditis,  diphtheritic,   143. 
Endocarditis,  malignant,  143. 
Endocarditis,  mycotic,   143. 
Endocarditis,  simple,  143,  150,  157. 
Endocarditis,  ulcerative,  143,  154,  163; 
course  of,  172; 
diagnosis  of,   179; 
morphine  in,   196; 
treatment  of,  191. 
54 


Endocarditis,   vegetative,   143. 

J<]ndocar(litis,   vcrrucoso,    143. 

Endocardium,  diseases  of,  143. 

Enteric  fever.     (See  Fever.) 

Epilepsy,  in  mitral  stenosis,  212. 

Ewart's  sign,  in  pericarditis  with  effu- 
sion, 80,  81. 

Exercise,  in  dilatation,  592; 
resistance,   455,   592 ; 
in  valvular  lesions,  414,  454,  502. 

Expectoration,    in    aneuiysra    of    tho- 
racic aorta,  784. 

Fatty  heart,  599; 

aperients  in,  612; 

camphor  in,  611; 

case  of,  607 ; 

diagnosis  of,  605; 

diet  in,  608; 

digitalis  in,  611; 

etiology  of,  600; 

gentian  in,  6i0; 

gluttony,  predisposing  to,  601 ; 

hypophosphites  in,  610; 

inspection  in,  604; 

iron  in,  610; 

morbid  anatomy  of,  599; 

nitroglycerin  in,  611; 

nux  vomica  in,  610; 

orthopnoea  in,  603; 

palpation  in,  604; 

pathology  of,  599; 

percussion  in,  604; 

physical  signs  in,  604; 

prognosis  in,  606; 

strophanthus  in,  611; 

strychnine  in,  Gil ; 

symptoms  of,  602 ; 

treatment  of,  606. 
Fever,  in  pericarditis,  dry,  51; 

in  pericarditis,  with  effusion,  89; 

enteric,   in   endocarditis,    154; 

rheumatic,    indicating    acute    endo- 
carditis, 157 ; 

scarlet,     Cheyne-Stokes     respiration 
in,  617;    ' 

in  myocarditis,  522 ; 

leading  to  acute  endocarditis,  154; 

leading    to    pericarditis    with    effu- 
sion, 72. 
Fever,    typhoid,    Cheyne-Stokes   respi- 
ration in,  617; 

diagnosis  of,  differential,  from  acute 
endocarditis,  182; 

in  bradycardia,  625; 

in  endocarditis,  acute,  151. 


842 


DISEASES  OF   THE   HEART 


Fever,  in  myocarditis,  acute,  508; 

in  myocarditis,  clironic,  522; 

typhoid,  in  pericarditis,  acute,  40; 

treatment  of,  in  acute  myocarditis, 
516. 
Fibroma,  of  myocardium,  lUUi. 
First  rib  sign,  in  pericarditis  with  ef- 
fusion, 75. 
Foetal  life,  acute  endocarditis  in,  143; 

developmental  anomalies  in,  (i!)(); 

perforate     interventricular     sieplum 
in,  (iSS. 
Fomentations,  in  pericarditis,  88. 
Food,  in  valvular  lesions,  428. 
Fragmentation  of  myocardium,  088. 
"  Fremissement  calairc,"  in  mitral  ste- 
nosis, 259. 
Friedreich's  sign   in   adlierent   i)ericar- 

dium,  120. 
Friction-sounds.    (Sec  Sounds.) 
Functional   disorders,  70:3; 

cases  of,  705,  714; 

digitalis  in,  709; 

neuroses  in,  703; 

strophantlius  in,  711 ; 

stryclinine  in,  709; 

tuberculosis  in,  710. 

Gangrene   of   foot,   in   arterial    throm- 
bosis,  070 ; 
of  leg,  in  mitnil  rcgiirgitalion.  238. 
Gastritis,  chronic,  in  chronic  myocai'- 

ditis,  551. 
Gelatin,    injection    of,    in    aneurysm, 

787. 
Germs.      (See  IMicro-organisms.) 
Glonoin,  in  valvular  disease,  432,  440. 
Gluttony,  inducing  fatty  lu'art,  001. 
Goitre,  exophtiialmie,  hypertrophy  in, 
570 ; 
tachycardia  in,  715. 
Gonorrh(ra.  in  a(  iite  endocarditis,  154, 
181; 
in  acute  myocarditis,  508. 
Gout,  in  mitral  stenosis,  254; 
in  regurgitation,  aortic.  2S0,  290. 

Habits,   in    valvular  lesions,   410,   420, 

470. 
Ha-mopcricardiiim,  130. 
lla'nutphiliii.  in  acute  pericarditis,  47. 
Heart,  area,  aortic,  3; 

mitral,   4; 

pulnuinic.  3; 

tricusjiid,  3. 
Heart,  atrophy  of.     (See  Atrophy.) 


Heart,  auscultation  of,  12; 

deep  boundaries  of,  0; 

dilatation  of   (see  Dilatation); 

diseases  of,  congenital,   086; 

disorders  of,  functional,  703; 

enlargement  of,  5 ; 

fatty   (see  Fatty  Heart)  ; 

]iy])crtrophy  of    (see  Hypertrophy) ; 

location  of,  1 ; 

imisical,  notable  example  of,  30; 

])()sition  of,  attempt  to  fix,  2; 

relation     of,     to     anterior     thoracic 
wall,   1; 

size  of,  how  ascertained,  5; 

valve  lesions  of  the  right,  summary 
of  physical  signs  of,  389 ; 

vessels  and  valves,  position  of,  3. 
Heart  sounds.     (See  Sounds.) 
Hemiplegia,  embolic,  in  acute  endocar- 
ditis,  1,58,  184.' 
Heroin,   in   pericarditis   with   elfusion, 

88. 
Home    surroundings,    in    valvular    le- 
sions, 410. 
Ilydropericardium,  103,  127,  131; 

diagnosis  of,  129; 

dropsy  in,   1.30; 

etiology  of,  128; 

inspection  in,   128; 

morbid  anatomy  of,  127; 

palj)ation  in,  128; 

percussion  in,  129; 

physical   signs  in,   128; 

])rognosis  in,  129; 

])yre\ia  in,  129; 

rlummatism  in,  129; 

sym])toms  of,  128; 

treatment  of,  129. 
Hypera^mia,  chronic,   110. 
Hy])notics,  in  valvular  disease,  500. 
lIypo])hosphites,  in  fatty  heart,  (ilO; 

in  valvular  lesions,  448. 
Hypertrophy  of  the  heart,  565; 

aconite,  not  used  in,  575; 

diagnosis  of,  572; 

digitalis   in,   575; 

etiology  of,  568; 

following  emphysema,  570; 

ins]iection  in,  571  : 

morbid  anatomy  of,  565; 

paljjation  in,  571 ; 

percussion  in,  571  ; 

physical   signs  in,  571; 

prognosis  in,  574; 

sym|)toms  of,  570; 

treatment  of,  575. 


INDEX 


843 


Ice,  in  paroxysmal  tachj'cardia,  736. 
Ice-bag,  in  acute  endocarditis,  189; 

in  pericarditis,  87,  S'J. 
Illnesses  in  valvular  lesions,  429. 
Inadequacy,  cardiac,  of  the  corpulent, 

599. 
Incoiiij)etency,   cardiac,   555. 
Individual  tendencies,  in  clnonic  endo- 
carditis, 20G. 
Infarction,  in  acute  endocarditis,  158; 

in  acute  myocarditis,  514. 
Infection,  affecting  valves,  185. 
Influenza,  in  dilatation,  577; 

in  acute  endocarditis,   151,   156; 

in  fatty  heart,  600; 

in  myocarditis,  chronic,  522,  551; 

in  paroxysmal  tachycardia,  732. 
Injection  of  gelatin  in  aneurysm,  787 ; 

of  gelatin  and  salt  solution,  812. 
Insomnia,     in     mitral     regurgitation, 
237; 

in   mitral   stenosis,   256. 
Insufficiency,  mitral.     (See  Mitral  In- 
sufficiency. ) 
Insurance,  life.     (See  Life  Insurance.) 
Iron,  in  fatty  heart,  610; 

in  insufficiency,  mitral,  597; 

in  myocarditis,  acute,  517; 

in  valvular  lesions,  448. 

Kidneys,  in  arteriosclerosis,  741 ; 
in  endocarditis,  acute,  150,  158,  185; 
in   endocarditis,   chronic,   203; 
in  myocarditis,  acute,  514; 
in  pericarditis,  acute,  45; 
in  pericarditis,  chronic,  112; 
in  regurgitation,  mitral,  238; 
in  valvular  disease,  490. 
Knowledge  of  lesion,  effect  on  patient, 

411. 
Kussmaul's  sign,  in  adherent  pericar- 
dium, 120. 
Kyphoscoliosis,  resulting  in  hypertro- 
phy of  right  ventricle,  570. 

Lesions,  valvular.      (See  Valvular  Le- 
sions.) 

Leucocytosis,    in    acute    endocarditis, 
181. 

Life   insurance,   relation   to,    of   prog- 
nosis in  valvular  disease,  412. 

Lipoma,  of  myocardium,  666. 

Liver,  cirrhosis  of,    102,    156; 
in   dilatation,   584 ; 
in     endocarditis,     acute,     156,     171, 
185. 


Liver,    in    pericarditis,    chronic,    100, 

102,  105,  109,  117,  122; 
in  pericarditis,  dry,  63; 
in   pericarditis,   with   effusion,   liigh 

position  of,  70; 
in   regurgitation,   aortic,  288; 
in  regurgitation,  mitral,  219,  233,  238; 
in  regurgitation,  tricuspid,  347,  350; 
in  stenosis,  nntral,  257,  268; 
in  valvular  disease,  405,  464; 
pseudo-,  Pick's  pericarditic,  123. 

Maculae  tendini.T,   101. 

Magnesia,    sulphate    of,    in    valvular 

disease,  447,  492. 
Malignant   endocarditis.      (See   Endo- 
carditis.) 
Marriage,  in  valvular  disease,  422. 
Massage,  in  chronic  myocarditis,  559. 
Measles,    resulting    in    acute    aortitis, 
760; 

resulting  in  acute  endocarditis,  154; 

resulting  in  acute  pericarditis,  46. 
Mechanical   devices   as   aids   to   deter- 
mining disease,   815. 
Mediastinitis,     associated     with     peri- 
carditis,  101. 
Mediastinopericarditis,    103,    104,    105; 

Perez's  sign  in,  121. 
Medicinal  agents,  in  valvular  disease, 

444. 
Micro-organisms,  in  abscess,  508; 

in  blood,  181; 

in  dilatation,  577; 

of   diphtheria,    151,    156; 

in  endocarditis,  acute,  144,  149,  150; 

gas   forming,    133; 

of  influenza,   151; 

in  myocarditis,  acute,  508: 

in  pericarditis,  acute,  40,  42; 

in  penumopericardium,   133; 

pyogenic,  149; 

of  tuberculosis,  42,  332; 

of  typhoid  fever,   151. 
Mitral  insufficiency,  relative,  594; 

chlorosis  in,  597; 

diagnosis  of,  596; 

digitalis  in,  598; 

etiology  of,  .594; 

iron  in,  597; 

nitroglycerin  in,  594; 

pathology  of,  594; 

physical  signs  in,  596; 

prognosis  in,  597 ; 

in   rheumatism,   595; 

symptoms   of,   596. 


su 


DISEASES  OP  THE   HEART 


Mitral  insufficienc-y,  troatnient  of.  597. 
Mitral    regurgitatii)U    (sec    Kegiirgita- 
tion) ; 

stenosis   (see  .Stenosis). 
Mode    and    causes    of    death.       (See 

Death.) 
Moderator  bands.  30. 
Morbus  ceruleus,  in  |)ulinonary  steno- 
sis, 385 
Morphine,    in    aneiuysni    of    thoracic 
aorta,  813; 

in  C'heyne-Stokes  respiration,  023; 

in  congenital  diseases,  093; 

in  dilatation,  r)l>3: 

in  endocarditis,   acute,   simple,    175; 

in  endocarditis,  ulcerative,  190; 

injection  of,  in  aneurysm,  814; 

in  myocarditis,  chronic,  533,  501 ; 

in  pericarditis,  dry,  09,  88,  91; 

in   pneumo])ericardium,    135; 

in    regurgitation,    aortic,    288,    290, 
310; 

in  stenosis,  aortic,  333; 

in  stenosis,  mitral,  272; 

in  Stokes- Adams  disease,  635; 

in  valvular  disease,  440,  481,  499. 
Murmurs,  accidental,  20,  32; 

differential  diagnosis  of,  34; 

not      accompanied      by      secondary 
changes,  35; 

detection  of,  13; 

endocardial,  21 ; 

exocardial,   36; 

musical,  29; 

pericardial,    effect    of    pressure    on, 
59; 

transmission     of,     25.        (See     also 
Sounds.) 
Muscle,   papillary,  degeneration    of,   a 
cause  of  mitral   insudicicncy,  596. 
Mycotic  endocarditis.      (See   Endocar- 
ditis.) 
Myocarditis,  acute,  505; 

antitoxin  in,  515; 

associated   with   endocarditis,   157; 

diagnosis  of,  514; 

digitalis  in,  510; 

diphtheria  in,  508,  511; 

etiology  of,  .508; 

infarction  in,   158; 

iron  in,  517; 

micro-organisms  in,  .508; 

morbid  anatomy  of,  506; 

palpation  in,  514; 

percussion  in,  514; 

in  physical  signs  in,  514. 


^Myocarditis,  prognosis  in,  515; 

l)ulse   in,  511,  513; 

rheumatism  in,  508,  513,  515; 

scarlatina   in,  508,  516; 

small-pox  in,  508; 

strophanthus  in,  516; 

symptoms  of,  510; 

treatment  of,  515; 

in  typhoid  fever,  508,  516. 
Myocarditis,  chronic,  518; 

atropine  in,  502; 

baths  in,  Turkish,  552; 

brandy  in,  501 ; 

Bright's    disease,     associated     with, 
539; 

bromides  in,  563; 

bronchitis,  acute,  in,  551; 

camphor  in,  561 ; 

cases  of,  .520,  531,  540,  541; 

chloralamide  in,  563; 

diagnosis  in,  122,  547; 

digitalis  in,  ,522,  564; 

dropsy  in,  530,  563; 

etiology  of,  522; 

gastritis,  chronic,  in,  551 ; 

influenza  in,  522,  .551; 

inspection  in,  543; 

massage  in,  559; 

morbid  anatomy  of,  519; 

morphine  in,  533,  561 ; 

nitroglycerin  in,  553,  560; 

palpation  in,  543; 

percussion  in,  544; 

physical  signs  in,  543; 

pneumonia   in,  551; 

])rognosis  in,  549; 

])ulse  in,  529; 

rheumatism  in,  522,  .541 ; 

strophanthus  in,  .553,  561; 

strychnine   in,  553; 

symptoms  of,  526; 

treatment  of,  551 ; 

typhoid  fever  in,  522. 
Myocardium,  cancer  of,  666; 

degeneration  of,  in  chronic  pericar- 
ditis, 101; 

diseases  of,  .505; 

fibroma  of,  600: 

fragmentation   of,  008; 

lipoma  of,  600; 

segmentation  of,  668. 
Myocardium,  syphilis  of,  663; 

diagnosis  of,  (»04; 

digitalis  in,  665; 

etiology  of,  003; 

iodides  in,  005. 


INDEX 


845 


Myocardium,  syphilis  of,  mercury  in,  I 
()();") ; 
morbid  anatomy  of,  003; 
prognosis  in,  005; 
symptoms  of,  004; 
treatment  of,  005. 

Nephritis,  in  acute  pericarditis,  44. 
Neuroses,  703,  717,  731; 

diagnosis   of,   724; 

etiology   of,    722; 

pain  in,  728; 

pathology  of,  703; 

prognosis  in,  720; 

symptoms  of,  704; 

treatment  of,  727. 
Nitroglycerin,  in  angina  pectoris,  058; 

in  aortitis,  acute,  702; 

in  arteriosclerosis,  757; 

in  dilatation,  591,  593; 

in  endocarditis,  chronic,  202; 

in  fatty  heart,  Oil; 

in  mitral  insufficiency,  594; 

in  myocarditis,  chronic,  553,  500; 

in  pseudo-angina  pectoris,  728; 

in  regurgitation,  aortic,  288,  314,310; 

in  stenosis,  aortic,  332,  333; 

in  stenosis,  mitral,  272; 

in  Stokes-Adams  disease,  635; 

in  tachycardia,  715; 

in  valvular  diseases,   442,  444,   440, 
488,  498. 

Occupation,  effect  of,  in  valvular  dis- 
eases, 409,  419,  470. 
CEdema,  in  mitral  stenosis,  250; 

in  valvular  diseases,  495; 

digitalis  in,  495. 
Orthopnoea,  in  fatty  heart,  003; 

in  pericarditis  with  effusion,  67. 
Oxygen,  in  acute  endocarditis,  191 ; 

in  Stokes-Adams  disease,  035. 

Pain,  in  aneurysm  of  thoracic  aorta, 
782; 

attack  of,  in  neuroses,  728; 

cardiac,    718; 

in  pericarditis,  dry,  49. 
Palpitation,  in  cardiac   neuroses,   727. 
Paroxysmal  tachycardia,  730; 

features  of,  732. 
Pathogenesis,  of  thrombi,  074. 
Pathology  of  angina  pectoris,  640; 

of  fatty  heart,  599; 

of  mitral  insufficiency,  594; 

of  neuroses,  703. 


Pathology    of   Stokes-Adams    disease, 

027; 
of  tachycardia,  731. 
Pectoris,    angina     (see     Angina     Pec- 
toris) ; 
pseudo-angina,  719. 
Percussion,  "abgcdilmpfte"  metliod,  7 ; 
auscultatory,  or  stcthoscopic,  8; 
palpatory,  10. 
Perez's    sign    in    chronic    mediastino- 

pericarditis,   121. 
Pericarditis,  acute,  37; 
abscess  in,  47; 
alcoholism  in,  47; 
Bright's  disease  in,  45; 
bronchitis  in,  47; 
cancer  in,  47; 
caries  of  rib  in,  47; 
cholera  in,  40; 
diphtheria  in,  46; 
erysipelas  in,  40; 
etiology  of,  41; 
measles  in,  46; 
micro-organisms  in,  40,  42; 
morbid  anatomy  of,  37; 
nephritis  in,  44; 
peritonaeum,  diseases  of,  in,  47; 
pleuritis  in,  47; 
pneumonia  in,  40; 
purulent  form,  40; 
purpura  heemoiThagica  in,  47; 
rheumatism  in,  42,  40; 
scarlatina  in,  46; 
scurvy  in,  47; 
serofibrinous  form,  40,  42; 
simplest  form,  37; 
small-pox  in,  46; 
strychnine  in,  516; 
suppurative  form,  42; 
tonsillitis  in,  44,  47; 

typhoid  fever  in,  4b; 

ulcer  in,  47; 

valvular  defects  resulting  from,  49. 
Pericarditis,  chronic,  99; 

baths  in,  110,  115; 

calomel  in,  125; 

cases  of,  105,  114,  123; 

compensation  prevented  in,  105; 

course  and  termination  of,   117; 

diagnosis   of,    122 ; 

diagnosis,   differential,  from  cirrho- 
sis of  liver,  122; 

digitalis  in,  126; 

diuretin  in,  126; 

etiology  of,  103 ; 

morbid  anatomy  of,  100. 


S^Q 


DISEASES  OF  THE  HEART 


Pericarditis,     chronic,     palpation     in, 
120; 

percussion  in,  121 ; 

pliysical  signs  in,  118; 

prognosis  in,   123; 

rheumatism  in,   117; 

stasis  in,  117; 

strophanthus  in,   114; 

strychnine  in,  114,  125; 

symptoms  of,   104; 

treatment  of,  124. 
Pericarditis,  dry,  48; 

cases  of,  oO,  52,  61 ; 

course  and  termination  of,  56; 

deglutition  in,  painful,  49; 

tliagnosis  of,  60; 

dili'erential,   60; 

digitalis  in,  54; 

inspection  in,  56; 

morplune  in,  69,  88,  91; 

pain  in,  49; 

palpation  in,  57; 

percussion  in,  57 ; 

])hysical  signs  in,  56; 

pneumonia  in,  60; 

prognosis  in,  61 ; 

pyrexia  in,  51 ; 

rheumatism  in,  50,  54,  61; 

strydinine  in,  53; 

symptoms  of,  48; 

hiiMuorrliagic,  40,  47. 
Pericarditis,  with  effusion,  64; 

anodynes  in,  88; 

atrojjine  in,  92; 

belladonna  in,  88; 

blister  in,  86,  87; 

calomel  in,  89; 

cases  of,  68,  70,  92; 

chloroform  in,  88; 

codeine   in,   88,   91; 

course  and  termination  of,  73; 

diagnosis  of,  81 ; 

dilFerential,  82; 

digitalis  in,  83; 

fever  in,  89; 

"first  rib"  sign  in,  75; 

fomentations  in,  88; 

lieroin  in,  88; 

ice-bag  in,  87,  89; 

inspection  in,  75; 

opium  in,  8S,  91 ; 

orthopnci-a  in,  67; 
percussion  in,  76; 
pliysical  signs  in,  74; 
I)rf)gnosis  in,  84 ; 
puncture  in,  site  of,  94,  96. 


Pericarditis,    resulting   from    pneumo- 
nia, 73; 
with   effusion,   resulting  from   scar- 
let fever,  72; 

rheumatism  in,  68,  70,  73,  84; 

sepsis  in,  72; 

signs  in,  "first  rib,"  75; 

Ewart's,  80,  81; 

Pins',  80; 

Kotch's,  78; 

strychnine  in,  91 ; 

symptoms  of,  64; 

treatment  of,  86,  90; 

tuberculosis  in,  84. 
Periarteritis   nodosa,    769; 

etiology  of,  7(i9 ; 

morbid  anatomy  of,  769; 

prognosis  in,  770; 

sepsis  in,  769; 

symptoms  of,  769; 

treatment  of,  770. 
Pericardium,  adherent,  99; 

bacteria  in,  45; 

signs  in,  l^roadbent's,  119; 

Friedreich  "s,  120; 

Kussmaul's,  120. 
Pericardium,  carcinoma  of,   141 ; 

diseases  of,  37 ; 

perforated  by  gastric  ulcer,  133; 

sarcoma  of,  141; 

syphilis  of,  139; 

tubercidosis  of,  136. 
Pick's  pcricarditic  pseudo-cirrhosis  of 

the   liver,    123. 
Pins'   sign,   in   pericarditis   with   ellu- 

sion,  80. 
Pleurisy,  mistaken  for  pericarditis,  83. 
Pneumonia,  in  aortitis,  acute,  760; 

in   bradycardia,    625; 

in  Cheyne-Stokes  respiration,  617; 

in  endocarditis,  acute,  185; 

croupous,  154,  156,  181; 

recovery  from,  155; 

in  myocarditis,  chronic,  551 ; 

in  pericarditis,  acute,  46; 

in   pericarditis,  chronic,  103; 

in  pericarditis,  dry.  60; 

in  pericarditis,  with  efTusion,  73,  97; 

in   regurgitation,   mitral,   224; 

in   stenosis,  aortic,  341 ; 

in  valvular  disease,  440. 
Pneumopericardium,  132 ; 

bacilli  in,  gas  forming,  133; 

brandy  in.  135; 

cases  of,  133; 

diagnosis  of,  135. 


INDEX 


847 


Pneumopericardium,  digitalis  in,  13G; 
etiology  of,   132; 
inspection  in,  134; 
morbid  anatomy  of,  132; 
morphine  in,  135; 
prognosis  in,  135; 
resulting  from  trauma,  133; 
resulting  from  ulcer,  133; 
strychnine  in,   130; 
symptoms  of,  133; 
treatment  of,  135. 
Pregnancy,   in    valvular   defects,    409, 

422. 
Pressure,  effect  of,  on  pericardial  mur- 
mur, 59. 
Pseudo-angina  pectoris,  719; 

-ciri'hosis    of    liver,    Pick's    pericar- 
ditis,  123. 
Pulmonary    artery,    stenosis    of     (see 

Stenosis). 
Pulmonary      regurgitation      (see    Re- 
gurgitation) ; 
stenosis  (see  Stenosis). 
Pulse,   capillary,   in  aortic   regurgita- 
tion, 301; 
inequality   of,   in   aortic    aneurysm, 

801; 
inequality    of,    in    mitral    stenosis, 

257,  259,  260; 
instability  of,  in  acute  myocarditis, 

511,  513; 
tension   of,   in   chronic   myocarditis, 

529; 
venous,  in  aortic  regurgitation,  301 ; 
"  water  hammer,"  in  aortic  regurgi- 
tation, 298. 
Puncture,  site  of,  in  pericarditis  with 

effusion,  94,  96. 
Pyrexia,  in  endocarditis,  acute,   171; 
in  hydropericardium,  129; 
in  pericarditis,  dry,  51; 
in  regurgitation,  tricuspid,  346. 

Quincke's    sign,    in    aortic    regurgita- 
tion, 298. 

Regurgitation,   aortic,  278; 
alcoholism  in,  280; 
cases  of,  282,  288,  293,  308,  313; 
cusp,  ruptured  in,  278; 
diagnosis  of,  305; 
digitalis  in,  288,  290; 
Duroziez's  sign  in,  305; 
etiology  of,  280; 
gout  in,  280,  296; 
inspection  in,  288,  290,  316. 


llegurgitation,  aortic,  nitroglycerin  in, 
288,  314,  316; 

palpation  in,  298; 

percussion  in,  301 ; 

physical  signs  in,  297; 

prognosis  in,  300; 

pulse  in,  298,  301; 

(Quincke's  sign  in,  298; 

rheumatism  in,  289; 

scarlatina  in,  309 ; 

strophanthus  in,  288,  291; 

strychnine  in,  290,  316; 

symptoms   of,  282; 

syphilis  in,  284. 
Regurgitation,  aortic  and  mitral,  com- 
bined, 397; 

diagnosis  of,  391,  397; 

prognosis  in,  398; 

symptoms  of,  397. 
Regurgitation,  aortic,  and  aortic  ste- 
nosis combined,  396. 
Regurgitation,  aortic,  and  mitral  ste- 
nosis  combined,   393; 

inspection  in,  395; 

palpation  in,  395; 

pei'cussion  in,  395; 

prognosis  in,  394,  396; 

symptoms  of,  393. 
Regurgitation,  mitral,  216; 

Brighfs  disease  in,  237; 

cases  of,  224,  229,  232,  247; 

congestion  in,  237; 

diagnosis  of,  245; 

digitalis  in,  225; 

dropsy  in,  219,  236,  245; 

dyspnoea  in,  238,  257; 

etiology  of,  252; 

inspection  in,  239; 

insomnia  in,  237; 

morbid  anatomy  of,  216; 

palpation  in,  239; 

percussion  in,  240; 

physical  signs  in,  239; 

pneumonia  in,  224; 

prognosis  in,  246; 

resulting  in  gangrene,   238; 

rheumatism  in,  222,  247; 

scarlatina  in,  222,  224,  229; 

stasis  in,  236; 

strychnine  in,  225; 

symptoms  of,  223; 

tuberculosis  in,  232. 
Regurgitation,  mitral,  and  aortic  ste- 
nosis combined,  396. 
Regurgitation,  mitral,  and  mitral  ste- 
nosis combined,  392. 


848 


DISEASES  OF  THE   HEART 


Regurgitation,  symptoms  of,  391. 
Regurgitation,    of    pulmonary    artery, 
772; 

diagnosis  of,  772. 
Regurgitation,  pulmonary,  305; 

case  of,  3G8; 

diagnosis  of,  387 ; 

etiology  of,  380. 

morbid  anatomy  of,  3G5; 

l)a]pation  in,  371 ; 

percussion  in,  371; 

physical  signs  in,  370; 

prognosis  in,   374; 

stasis  in,  367; 

symptoms   of,   367. 
Regurgitation,  tricuspid,  343; 

case  of,  354; 

cyant)sis  in,  347; 

diagnosis  of,  363; 

dropsy  in,  351 ; 

etiology  of,  350; 

inspection  in,  349; 

morbid  anatomy  of,  344; 

palpation  in,  350; 

percussion  in,  350; 

physical  signs  in,  349; 

prognosis  in,  354; 

pyrexia  in,  340; 

resulting    from    cirrhosis    of    lung, 
340; 

from  fibroid  phthisis,  346; 

from  renal  cirrhosis,  345; 

secondary     to     chronic     bronchitis, 
34G; 

stasis  in,  347; 

symptoms  of,  347. 
Rheunuitism,    acute,    in    bradycardia, 
625 ; 

in  endocarditis,  acute,  146,  181,  186; 

in  endocarditis,  chronic,  522; 

in  myocarditis,  acute,  513,  515; 

in  pericarditis,  acute,  42; 

in  pericarditis,  chronic,   117; 

in  pericarditis,  dry,  50,  54; 

in  regurgitation,  aortic,  289; 

in  regurgitation,  mitral,  222; 

in  stenosis,  pulmonary,  377; 

in  tachycardia.  732; 

in  valvular  disease,  401,  429. 
Kheiimatism,   articidar,  32,  34; 

in  dilalafi(m.  583; 

in     endocarditis,     acute,     152,     157, 
187: 

in  liydro])ericardium,   129; 

in   mitral    insudiciency,  595; 

in  myocarditis,  acute,  508. 


Rheumatism,  articular,  in  pericarditis, 
acute,   42 ; 
in  pericarditis,  dry,  61; 
in  pericarditis,  with  effusion,  70; 
in  regurgitation,  mitral,  247 ; 
in  stenosis,  pulmonary,  376; 
in  stenosis,  tricuspid,  356; 
in  valvular  disease,  441,  479,  485. 
Rheumatism,   inflammatory,   in   endo- 
carditis, acute,  153; 
in  myocarditis,  chronic,  541 ; 
in  pericarditis,  with  efTusion,  68,  73, 

84; 
in  stenosis,  mitral,  274; 
in  valvular  disease,  436,  441. 
Rhythm,  gallop  or  canter,  18; 

a  sign  of  the  end,  20. 
Rotch's  sign,  in  pericarditis  with  efTu- 
sion, 78. 

Scarlatina,  in  aortitis,  acute,  760; 
in   congenital    disease,   698; 
in  endocarditis,  acute,  154; 
in  myocarditis,  acute,  508,  516; 
in  pericarditis,  acute,  46; 
in  regurgitation,  aortic,  309 ; 
in    regurgitation,    mitral,    222,    224, 

229; 
in  si'cnosis,  mitral,  274; 
in  stenosis,  tricuspid,  358. 
Scarlet  fever.     (See  Fever.) 
Sclerosis,  246,  286,  573. 
Scurvy,  in  pericarditis,  acute,  47. 
Second   sound,  simulated  doubling  of, 

17. 
Segmentation     of     the     myocardium, 

668. 
Sepsis,  in  acute  endocarditis,  170,  193; 
in  periarteritis  nodosa,  769 ; 
in  pericarditis  with  effusion,  72. 
Septica'mia,     in     acute     endocarditis, 

155,   156. 
Serum,  anti-streptococcus,  in  acute  en- 
docarditis, 193. 
Signs,   Rroadbent's,   in   adherent   peri- 
cardium,  119; 
Duroziez's,   in   aortic   regurgitation, 

305; 
Ewart's,    in    pericarditis   with    efTu- 
sion, SO,  81: 
"  first  rib,"  in  pericarditis  with  efTu- 
sion, 75 ; 
Friedreich's,     in     adherent     pericar- 
dium, 120; 
Kussmaul's,     in     adherent     pericar- 
dium, 120. 


INDEX 


849 


Signs,  Perez's,  in  chronic  mediastino- 
pericarditis,  121; 

Pins',  in  pericarditis  with  effusion, 
80; 

Quincke's,    in    aortic    regurgitation, 
298; 

Rotch's,    in   pericarditis    with    effu- 
sion, 78. 
Simple  endocarditis.      (See  Endocardi- 
tis.) 
Sraallness  of  arteries,  congenital,  773. 
Small-pox,  in  acute  endocarditis,  154; 

in  acute  myocarditis,  508; 

in  acute  pericarditis,  4G. 
Sound-friction,    intensity   of,   59; 

location  of  the  pericardial,  58; 

quality  of,  59; 

rhythm  of,  58. 
Sounds,  heart,  normal,   13; 

reduplication  of,  IC,  18; 

second,  simulated  doubling  of,   17. 
Spleen,  abscess  of,  in  acute  endocardi- 
tis, 150,  185. 
Stasis  in  pericarditis,  chronic,  117; 

in  regurgitation,  aortic,  297 ; 

in  regurgitation,  mitral,  23G; 

in  regurgitation,  pulmonary,  367; 

in  regurgitation,   tricuspid,   347; 

in  stenosis,  mitral,  257 ; 

in  stenosis,  tricuspid,  358. 
Stenosis,  of  aorta,  770; 

symptoms  of,  771; 

treatment  of,  772. 
Stenosis,  aortic,  319; 

cases  of,  323,  330,  339; 

cyanosis  in,  335; 

diagnosis  of,  338; 

digitalis  in,  326; 

inspection  in,   335; 

morbid  anatomy  of,  319; 

nitroglycerin  in,  332,  333; 

palpation  in,  335; 

percussion  in,  336; 

physical   signs   in,   335; 

pneumonia  in,  338; 

prognosis  in,  339; 

strychnine  in,  332 ; 

symptoms  of,  323. 
Stenosis,  aortic  and  mitral  combined, 
392; 

diagnosis  of,  392; 

prognosis  in,  393 ; 
symptoms  of,  392. 
Stenosis,  mitral,  249; 
bronchitis  in,  256; 
cases  of,  253,  263,  270,  273. 


Stenosis,  mitral,  delirium  in,  270; 
diagnosis  of,  208; 

digitalis  in,  272; 

epilepsy  in,  212; 

"  fremissement  cataire  "  in,  259; 

gout  in,  254; 

insomnia  in,  256; 

inspection  in,  258; 

morbid  anatomy  of,  249; 

morphine  in,  272; 

nitroglycerin  in,  272; 

oedema  in,  256; 

palpation  in,  259; 

percussion  in,  260; 

physical  signs  in,  258; 

prognosis  in,  269; 

pulse  in,  257,  259,  260; 

rheumatism  in,  264; 

scarlatina  in,  274; 

stasis  in,  257; 

strophanthus  in,  272; 

strychnine  in,  272; 

symptoms  of,  255; 

syphilis  in,  254. 
Stenosis,   mitral,   and   pulmonary   ste- 
nosis combined,  387. 
Stenosis,  pulmonary,  376; 

eases  of,  377,  380; 

diagnosis  of,  373; 

inspection  in,  385; 

morbid  anatomy  of,  376; 

percussion  in,  386; 

physical  signs  in,  385; 

prognosis  in,  374; 

rheumatism  in,  376,  377; 

symptoms  of,  380; 

tuberculosis  in,  380. 
Stenosis,  of  pulmonary  artery,  772. 
Stenosis,  tricuspid,  355; 

cases  of,  379,  380; 

diagnosis  of,  353; 

digitalis  in,  359; 

inspection  in,  361 ; 

morbid  anatomy  of,  355; 

percussion  in,  362; 

physical  signs  in,  361 ; 

prognosis  in,  364; 

rheumatism  in,  356; 

scarlatina  in,  358; 

stasis  in,  358; 

symptoms  of,  357. 
Stokes- Adams  disease,  627; 

cases  of,  628.  630,  632; 

digitalis  in,  636; 

etiology  of,  627; 

morphine  in,  635. 


850 


DISEASES  OF  THE   HEART 


Stokes-Adams     disease,     uitroglycerin 
in,  635; 

oxygen  in,  035 ; 

pathology  of,  (i27; 

prognosis  in,  635; 

symptoms  of,  629; 

syphilis  in,  628; 

treatment  of,  635. 
Strophanthns.  in  angina  pectoris,  662; 

in  arterioselerosis,  757 ; 

in  endocarditis,  acute,  169; 

in  fatty  heart,  611 ; 

in  functional  disorders,  711; 

in  myocarditis,  acute,  516; 

in  myocarditis,  chronic,  553,  561; 

in  pericarditis,  chronic,  114; 

in  regurgitation,  aortic,  288,  291; 

in  stenosis,  mitral,  272; 

in  vahndar  disease,  432. 
Strychnine,  in  aortitis,  acute,  762; 

in  dilatation,  591 ; 

in  endocarditis,  acute,  169,  191; 

in  endocarditis,  chronic,  202; 

in  fatty  heart,  611; 

in  functional  disorders,  709 ; 

in  myocarditis,  chronic,  553; 

in  pericarditis,  acute,  516; 

in  pericarditis,  chronic,  114,  125; 

in  pericarditis,  dry,  53; 

in  pericarditis,  with  effusion,  91; 

in  pneuniopericardiuni,  136; 

in  regurgitation,  aortic,  290,  316; 

in   regurgitation,  mitral,   225; 

in  stenosis,  aortic,  332; 

in  stenosis,  mitral,  272; 

in  tachycardia,  736 ; 

in  valvular  disease,  439,  443,  445. 
Syncope,  in  aortic  regurgitation,  287. 
Syphilis,  in  aneurysm,  778,  795; 

in  arterioscleiosis,  742 ; 

in  angina  pectoris,  646; 

in  endocanlitis,  chronic,  204;' 

in  regurgitati(m,  aortic,  284; 

in  stenosis,  mitral,  254; 

in  stenosis,  tricuspid,  356; 

in  Stokes-Adams  disease,  628; 
Syphilis  of  the  myocardium,  663; 

of  the  ])ericar(liunK  139. 
Syphilis  vs.  rheumatism,  in  aortic  ste- 
nosis, 388. 
Syphilitic  arteritis,  764, 

Tachycardia,  730; 
calleine  in,  736; 
diagnosis  of,  734; 
digitalis  in,  736; 
diphtheria  in,  732. 


Tachycardia,  etiology  of,  732; 

ice  in,  736; 

inlluenza  in,  732; 

malaria  in,  732 ; 

nitroglycerin  in,  715; 

pathology  of,  731; 

prognosis  in,  735; 

rheumatism   in,  732; 

strychnine  in,  736; 

treatment  of,  735. 
Temperaments,  of  cardiopaths,  408. 
Tendencies,  individual,  2U6. 
Terrain  cure,  in  valvidar  disease,  454. 
Thoracic  aorta,  aneurysm  of,  775. 
Thoracic  cavity,  1. 
Thrombi,  ball,  674; 

bibliography  of,  680; 

cases  of,  676,  680; 

diagnosis  in,  677;' 

etiology  of,  674; 

pathogenesis  of,  674. 
Thrombi,  pedunculated,  674; 

prognosis  in,  678; 

symptoms  of,  675; 

ti-eatment  of,  678. 
Thrombosis,     arterial,     causing     gan- 
grene, 676; 

venous,  in  valvular  disease,  208. 
Tissue,  adipose,  in  syphilis  of  pericar- 
dium, 139. 
Tonics,  accessory,  499; 

cardiac,  441 ; 

nerve,  517. 
Tonsillitis,  in  endocarditis,  acute,  156; 

in  pericarditis,  acute,  44,  47. 
Tonometer,  Gaertner's,  826. 
Tricuspid  regurgitation    (see  Regurgi- 
tation) ; 

stenosis  (see  Stenosis). 
Tuberculosis,  of  pericardium,  136; 

of  lungs,   103. 
Tuberculosis,     p\ilmonary.     in     aneu- 
rysm,  808; 

in  dextrocardia,  681 ; 

in  functional  disorders,  716; 

in  pericarditis,  with  cfTusion,  84; 

in  regurgitation,  mitral,  232; 
in   stenosis,  pidmonary,  380; 
in  valvular  disease,  406. 
Typhoid  fever,  in  pericarditis,  46. 
Typhus,  in  acute  myocarditis,  508. 

Ulcerative   endocarditis.      (See   Endo- 
carditis.) 

Valvular  lesions  combined,  390; 
atropine  in,  500. 


INDEX 


851 


Valvular  lesions,  baths   in,  Naulieim, 

427,  404,  503; 
batlis  iu,  saline,  4GG; 
cail'cine  in,  432; 
calomel  in,  432,  44S,  491,  493; 
cases  of,  393,  436,  440,  469,  479,  482, 

485; 
cathartics  in,  492; 
chloral  hydrate  in,  501 ; 
chloralo.se  in,  501 ; 
change  of  climate  in,  432; 
clotliing  in,  425,  470 ; 
compensation  imperfect  in,  435; 
compensation  lost  in,  478; 
compensation  perfect  in,  413; 
complicated  with  catarrh,  bronchial, 

407; 
with  dropsy,  470; 
with  pneumonia,  440; 
with  rheumatism,  406; 
convallaria  in,  432,  497; 
diet  in,  428,  470; 
digitalis  in,  394,  430,  480; 
drugs  in,  430; 
exercise  in,  414,  454,  502; 
exercise,  resistance,  in,  455; 
glonoin  in,  432,  446; 
habits- in,  410,  420,  476; 
haematics  in,  448; 
home  surroundings  in,  410; 
hypnotics  in,  500; 
illnesses  in,  429. 


Valvular  lesions,  jalap  in,  493; 

marriage  in,  422; 

medicinal  agents  in,  444; 

mercury  in,  432; 

morphine  in,  440,  4S1,  499; 

nitroglycerin  in,  442,  444,  446,  488, 
498; 

occupation  in,  409,  419,  476; 

oedema  in,  495; 

pregnancy  in,  409; 

prognosis  in,  401 ; 

rest  in,  448,  502; 

rheumatism   in,   401,   429,   436,   441, 
479,  485; 

strophanthus  in,  432; 

strychnine  in,  439,  443,  445; 

Terrain  cure  in,  454; 

treatment  of,  413,  435,  478; 

tuberculosis  in,  406. 
Vegetative   endocarditis.      (See   Endo- 
carditis.) 
Verrucose    endocarditis.       (See    Endo- 
carditis.) 
Vessels  and  valves  of  heart,   position 
of,  3. 

Whisky,      in       acute       endocarditis, 
192; 
in  angina  pectoris,  660; 
in  pseudo-angina,  728; 
in  myocarditis,  chronic,  561; 
in  valvular  disease,  493. 


(4) 


THE   EIS"D 


ADDENDUM 


Recent  Important  Discoveries  Concerning  the  Mechanical  Effects  of 
Aortic  Regurgitation  upon  the  Cardio-vascular  System. 

Under  the  caption  of  Experimental  and  Clinical  Investigation 
of  the  Pulse  and  Blood  Pressure  Changes  in  Aortic  Insufficiency, 
there  appeared  in  The  Archives  of  Internal  Medicine,  Vol.  I, 
JSTo.  1,  January  15,  1908,  a  contribution  to  the  knowledge  of  this 
valvular  lesion  of  such  wide-reaching  significance  that,  if  confirmed 
by  other  physiologists,  it  is  destined  to  cause  a  rewriting  of  the 
chapters  devoted  to  this  subject  in  medical  text-books.  On  this 
account  I  cannot  permit  this  third  edition  to  be  given  to  the  pub- 
lic without  a  brief  statement  of  the  facts  discovered  by  Dr.  Hugh 
A.  Stewart  in  the  physiological  laboratory  of  Johns  Hopkins  Hos- 
pital. Inasmuch  as  this  present  edition  has  already  come  from 
the  press  and  only  awaits  binding,  it  has  been  decided  to  incor- 
porate these  novel  facts  in  an  addendum  rather  than  to  leave 
them  unnoticed.  There  is  the  additional  advantage  that  by  so 
doing  I  shall  leave  for  the  reader  the  original  and,  as  it  were, 
historical  conception  of  the  disease  which  has  dominated  medical 
thought  since  the  time  of  Corrigan,  that  he  may  contrast  the  dif- 
ferences between  Corrigan's  and  Stewart's  explanation  of  the  phe- 
nomena observed. 

By  a  reference  to  Chapter  VIII  it  will  be  seen  that  the 
pathology  of  aortic  regurgitation  is,  briefly,  as  follows :  Insuffi- 
ciency of  the  aortic  semilunar  valves  causes  a  portion  of  the 
blood  discharged  into  the  artery  during  systole  to  leak  back  into 
the  ventricle  with  the  next  ensuing  diastole.  The  quantity  of 
blood  thus  regurgitating  depends  upon  the  degree  of  damage  sus- 
tained by  the  valve,  but  whether  small  or  great  produces  collapse 
of  the  pulse  and  a  proportionate  dilatation  of  the  ventricle,  since 
the  regurgitating  stream  enters  the  cavity  of  the  ventricle  during 
its  period  of  diastole.     This  primary  dilatation  is  soon  counter- 

853 


854  DISEASES  OF  THE  HEAKT 

balanced  bv  hypertropby  of  the  wall,  in  consequence  of  wliicli 
the  powerful  and  capacious  ventricle  is  enabled  to  discharge  with 
abnormal  suddenness  the  increased  volume  of  blood  it  has  received 
from  both  auricle  and  aorta.  This  large  blood  wave  rapidly  dis- 
tends the  arteries  during  cardiac  systole  and  then  ra])i(lly  recedes 
during  diastole  because  of  the  regurgitation,  thus  giving  rise  to 
the  collapsing  jjulsc  and  other  vascular  phenomena  characteristic 
of  aortic  incompetence. 

lentil  Stewart's  careful  studies  proved  the  inaccuracy  of  Cor- 
rigan's  explanation  of  the  colla])se  of  the  pidse  this  had  seemed 
to  account  for  the  clinical  changes  fully  and  satisfactorily.  Now, 
however,  the  manner  in  which  the  mechanical  effects  on  the  heart 
and  pulse  are  produced  is  found  to  be  quite  different  and  to  pos- 
sess therapeutic  and  prognostic  importance.  For  a  description  of 
the  mechanical  devices  by  which  were  v(^^''*i'<lc'^  blood-pressure 
changes  in  the  ventricle  and  aorta,  as  well  as  the  ventricular  vol- 
ume curves  of  the  normal  heart  previously  described  by  Hender- 
son, the  reader  is  referred  to  Stewart's  original  thesis.  Space 
here  forbids  more  than  a  summary  of  his  conclusions,  but  it  may 
be  said  that  his  experiments  made  on  the  dog's  heart  are  pro- 
fusely illustrated  by  tracings  and  appear  convincing  as  to  their 
accuracy  and  thoroughness. 

In  the  first  place,  by  means  of  Henderson's  plethysmogra]ih 
he  studied  the  volume  curve  of  the  normal  ventricle  and  contirmed 
that  investigator's  conclusions ;  namely,  that  the  cardiac  cycle  is 
not  di})hasic  but  triphasic  and  consists  of:  (1)  systole,  or  the 
period  of  contracticm  and  discharge;  (2)  diastole,  or  the  period 
of  relaxation  and  filling;  (3)  diastasis,  or  period  of  rest.  These 
studies  showed,  furthermore,  tliat  an  acceleration  of  the  heart's 
rate  is  at  the  expense  of  the  period  of  rest,  not  of  systole  or  diastole, 
since  the  rapidity  with  which  the  ventricle  fills  is  invariable  for 
each  heart  and  is  independent  of  its  rate  of  contraction.  Conversely, 
slowing  of  the  heart  by  vagus  stiuiulatiou  lengthens  diastasis,  or 
the  period  of  rest,  and  does  not  affect  either  systole  or  diastole. 
If  ihe  heart  rate  is  accelerated  up  to  the  ])oint  of  total  abolitiou 
of  diastasis  tlie  systolic  output  per  unit  of  tiuie,  the  work  of  the 
heart,  and  the  mean  jiressure  in  the  aortic  system  are  increased. 
If  now  the  rate  of  the  heart  is  still  further  accelerated  the  ])eriod 
of  diastole  becomes  encroached  upon  1)V  tlie  succeeding  systole, 
complete  filling  is  prevented,  and  the  auiount  of  blood  difscharged 
with  each   systole   is   lessened.      The;   work  of  the   heart   is   not 


ADDENDUM  855 

greater,  for,  notwithstanding  the  increase  in  rate,  the  amount  of 
blood  discharged  in  a  given  unit  of  time  remains  as  before. 

Stewart  next  obtained  a  record  of  the  volume  curve  after  the 
aortic  valves  had  been  ruptured  by  means  of  McCallum's  valvu- 
lotome. These  tracings  (the  heart's  rate  in  the  two  instances  re- 
maining the  same)  Avere  then  laid  one  upon  the  other  and  com- 
pared. It  was  then  found  that  the  systole  of  the  ventricle  after 
aortic  regurgitation  had  l)een  jjroduced  did  not  occur  more  qulcldy, 
hut  more  sloivly,  requiring  for  its  completion  .22  of  a  second  in- 
stead of  .18  of  a  second,  as  when  the  heart  was  normal.  It  was 
also  ascertained  that  the  amount  of  blood  discharged  with  each 
systole  was  increased  over  the  normal  by  only  .5  c.c. 

This,  as  pointed  out  by  Stewart,  is  at  variance  Avith  the  teach- 
ings concerning  the  immediate  effect  on  the  ventricle  of  aortic 
regurgitation,  for  in  the  animal  experimentation  it  was  shown 
that  even  with  the  most  extensive  incompetence  only  a  fractional 
part  of  the  blood  regurgitated  and  that  the  ventricle  did  not  con- 
tract more  suddenly  and  rapidly  but  more  slowly  than  in  health. 
Moreover,  it  was  ascertained  that  the  lengthening  of  the  systole 
was  made  up  by  a  more  rapid  rate  of  filling  during  the  first  part 
of  diastole,  until  in  fact  the  ventricle  had  received  about  one 
fifth  of  its  supply. 

But  still  other  surprises  were  disclosed.  It  is  known  that 
there  is  a  certain  amount  of  residual  blood  left  in  a  ventricle 
when  in  a  state  of  dilatation,  and  hence  if  aortic  incompetence 
causes  left  ventricular  dilatation  this  should  lead  to  retention  of 
blood  in  the  ventricle.  It  was  found,  however,  that  despite  a 
slightly  increased  filling  the  ventricle  emptied  itself  more  com- 
pletely than  normally.  There  was  then  no  distention,  and  this 
was  taken  as  a  proof  of  increased  tonus  of  the  ventricular  muscle. 
This  increased  tonus  could  only  be  due  to  the  fact  that  instead  of 
the  regurgitating  stream  acting  as  a  dilating  force,  the  incom- 
petence of  the  valve  permitted  a  transference  of  pressure  from  the 
aorta  to  the  interior  of  the  ventricle,  and  it  was  this  transfer  of 
pressure  from  aorta  to  ventricle  which  occasioned  the  increased 
ventricular  tonus.  Moreover,  this  tension,  which  results  from 
increased  ventricular  pressure,  produces  hypertrophy  as  the  pri- 
mary effect  of  aortic  regurgitation  and  not  dilatation,  as  is  usu- 
ally taught. 

Finally,  in  his  experiments  Stewart  discovered  that  simple 
irritation  of  the  depressor  nerves  of  the  ventricle  without  destruc- 


856  DISEASES  OF  THE   HEART 

tion  of  the  valves  was  followed  l)v  capillarv  dilatation  and  a 
veritable  eollapse  of  the  pulse  through  reflex  action  of  the  vaso- 
motor centers.  Then  studying  the  arterial  tracing  he  found  that 
the  collapse  of  the  jjulse  occurred  during  systole,  and  not  diastole, 
as  has  always  been  believed.  In  short  he  demonstrated  that  the 
collapse  is  of  vasomotor  origin  and  due  to  free  systolic  outflow 
into  tlie  capillaries,  and  not  at  all  to  regurgitation.  This  con- 
clusion was  corroborated  by  the  finding  that  whenever  he  inter- 
fered with  escape  of  blood  into  the  capillaries — e.  g.,  by  compres- 
sion of  the  abdouiinal  aorta — he  abolished  the  collapsing  character 
of  the  pulse,  although  this  manipulation  should  at  the  same  time 
have  increased  the  regurgitation.  Tn  this  connection  also  it  may 
be  stated  that  the  production  of  aortic  regurgitation  failed  to  raise 
systolic  blood  })ressure,  but  did  lower  the  diastolic  pressure,  which, 
together  with  the  capillary  dilatation,  is  ^  conservative  effort  on 
the  part  of  nature,  since  it  lessens  intraventricular  pressure  and 
also  regurgitation. 

That  the  facts  thus  Ijriefly  stated  must  possess  both  prognostic 
and  therapeutic  importance  goes  without  saying.  So  long  as  the 
left  ventricle  is  equal  to  the  development  and  maintenance  of  in- 
creased tonus,  and  the  elastic  arterioles  can  res]iond  to  the  vaso- 
dilatiug  stiuiulus  so  as  to  pcruiit  ready  flow  into  the  capillaries, 
compensatory  liy])ertro]ihy  jjersists  and  symptoms  are  nil.  Hence 
the  perfect  adjustuient  of  the  heart  seen  in  the  3'oung  in  whom  the 
lesion  is  the  result  of  endocarditis.  In  those,  on  the  other  hand, 
in  whom  the  aortic  valve  leaks  as  a  part  of  a  general  arterio- 
sclerosis which  by  invasion  also  of  the  coronaries  has  led  to  myo- 
cardial degeneration,  both  increased  ventricular  tonus  and  a  free 
systolic  outflow  into  the  capillaries  are  wanting  or  but  poorly 
maintained.  Hence  symptoms  are  apt  to  appear  early,  and  when 
once  manifest  to  persist,  or  increase  in  spite  of  treatment,  and 
sudden  death  is  the  rule. 

Therapeutically  two  suggestions  arise:  (1)  Since  digitalis  con- 
stricts tlie  arterioles  it  should  be  administered  cautiously  and  in 
conjunction  with  vasodilators,  or,  instead,  strophanthus  should  be 
the  drug  relied  upon  when  cardiac  inadequacy  appears.  (2)  Ni- 
trite of  sodium  or  some  other  equally  eflicient  vasodilator  is  called 
for,  tlieoretically  at  least,  wlicu  the  colla))sing  character  of  the 
|)ulse  is  not  well  iiiai'kcd,  aud  in  the  sclerotic  type  of  the  disease, 
should  always  be  pi-cscrilKMl. 


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